TY  - JOUR
AU  - Shirif, Abdulbaset Zidane
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Elaković, Ivana
AU  - Đorđević, Ana
AU  - Matić, Gordana
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4259
AB  - The modern lifestyle brings both excessive fructose consumption and daily exposure
to stress which could lead to metabolic disturbances and type 2 diabetes. Muscles are important
points of glucose and lipid metabolism, with a crucial role in the maintenance of systemic energy
homeostasis. We investigated whether 9-week fructose-enriched diet, with and without exposure to 4-
week unpredictable stress, disturbs insulin signaling in the skeletal muscle of male rats and evaluated
potential contributory roles of muscle lipid metabolism, glucocorticoid signaling and inflammation.
The combination of fructose-enriched diet and stress increased peroxisome proliferator-activated
receptors-  and -  and stimulated lipid uptake, lipolysis and  -oxidation in the muscle of fructosefed
stressed rats. Combination of treatment also decreased systemic insulin sensitivity judged by
lower R-QUICKI, and lowered muscle protein content and stimulatory phosphorylations of insulin
receptor supstrate-1 and Akt, as well as the level of 11 -hydroxysteroid dehydrogenase type 1
and glucocorticoid receptor. At the same time, increased levels of protein tyrosine phosphatase-1B,
nuclear factor- B, tumor necrosis factor- , were observed in the muscle of fructose-fed stressed rats.
Based on these results, we propose that decreased glucocorticoid signaling in the skeletal muscle
can make a setting for lipid-induced inflammation and the development of insulin resistance in
fructose-fed stressed rats.
PB  - Basel, Switzerland: MDPI
T2  - International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders
T1  - Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress
IS  - 13
VL  - 22
DO  - 10.3390/ijms22137206
SP  - 7206
ER  - 

@article{
author = "Shirif, Abdulbaset Zidane and Kovačević, Sanja and Brkljačić, Jelena and Teofilović, Ana and Elaković, Ivana and Đorđević, Ana and Matić, Gordana",
year = "2021",
abstract = "The modern lifestyle brings both excessive fructose consumption and daily exposure
to stress which could lead to metabolic disturbances and type 2 diabetes. Muscles are important
points of glucose and lipid metabolism, with a crucial role in the maintenance of systemic energy
homeostasis. We investigated whether 9-week fructose-enriched diet, with and without exposure to 4-
week unpredictable stress, disturbs insulin signaling in the skeletal muscle of male rats and evaluated
potential contributory roles of muscle lipid metabolism, glucocorticoid signaling and inflammation.
The combination of fructose-enriched diet and stress increased peroxisome proliferator-activated
receptors-  and -  and stimulated lipid uptake, lipolysis and  -oxidation in the muscle of fructosefed
stressed rats. Combination of treatment also decreased systemic insulin sensitivity judged by
lower R-QUICKI, and lowered muscle protein content and stimulatory phosphorylations of insulin
receptor supstrate-1 and Akt, as well as the level of 11 -hydroxysteroid dehydrogenase type 1
and glucocorticoid receptor. At the same time, increased levels of protein tyrosine phosphatase-1B,
nuclear factor- B, tumor necrosis factor- , were observed in the muscle of fructose-fed stressed rats.
Based on these results, we propose that decreased glucocorticoid signaling in the skeletal muscle
can make a setting for lipid-induced inflammation and the development of insulin resistance in
fructose-fed stressed rats.",
publisher = "Basel, Switzerland: MDPI",
journal = "International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders",
title = "Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress",
number = "13",
volume = "22",
doi = "10.3390/ijms22137206",
pages = "7206"
}

Shirif, A. Z., Kovačević, S., Brkljačić, J., Teofilović, A., Elaković, I., Đorđević, A.,& Matić, G.. (2021). Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress. in International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders
Basel, Switzerland: MDPI., 22(13), 7206.
https://doi.org/10.3390/ijms22137206

Shirif AZ, Kovačević S, Brkljačić J, Teofilović A, Elaković I, Đorđević A, Matić G. Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress. in International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders. 2021;22(13):7206.
doi:10.3390/ijms22137206 .

Shirif, Abdulbaset Zidane, Kovačević, Sanja, Brkljačić, Jelena, Teofilović, Ana, Elaković, Ivana, Đorđević, Ana, Matić, Gordana, "Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress" in International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders, 22, no. 13 (2021):7206,
https://doi.org/10.3390/ijms22137206 . .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Elaković, Ivana
AU  - Vojnović-Milutinović, Danijela
AU  - Nikolić-Kokić, Aleksandra
AU  - Blagojević, Duško
AU  - Matić, Gordana
AU  - Tappy, Luc
AU  - Đorđević, Ana
AU  - Brkljačić, Jelena
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4468
AB  - Background: Both fructose consumption and chronic stress contribute to the development of metabolic disorders.
The consequences of such combination are not fully understood.
Objective: We investigated whether fructose supplementation and chronic stress synergistically disturb hepatic lipid
and glucose metabolism. The role of energy sensing, redox, and inflammatory status during development of metabolic
disturbances was investigated.
Methods: Female Wistar rats, aged 2.5 mo, were divided into 4 experimental groups: control (C) fed a standard diet
(commercial food and drinking water); fructose (F) fed the same food and 10% fructose solution; stress (S) fed the
standard diet and subjected to chronic unpredictable stress and, stress + fructose (SF) combining conditions F and
S as above. Stress included daily stressors: cold water forced swimming, physical restraint, cold room, wet bedding,
rocking, switching, or tilting cages. After 9 wk, hepatic enzymes and transcription factors involved in gluconeogenesis,
lipogenesis, fatty acid oxidation, antioxidative defence, energy sensing, and cytokines were assessed by qPCR, Western
blotting, and spectrophotometry and analyzed by 2-factor ANOVA.
Results: Fructose increased AMP-activated protein kinase (AMPK) phosphorylation (40%; P < 0.05) and the ratio of
inhibitory phosphorylation to total acetyl-CoA carboxylase (46%; P < 0.01), and decreased sterol regulatory element
binding protein 1c nuclear translocation by 30% (P < 0.05) in F and SF compared with C rats. Increased phosPck
(phoenolpyruvate carboxykinase) (85%) and G6pase (glucose-6-phosphatase) (55%) was observed in S rats (P < 0.05).
A 40% decrease in Apob (apolipoprotein B-100) and an increase in hepatic lipids (P < 0.05), together with a double
increase in TNF-α (P < 0.001), were observed in S rats, but without liver histopathological changes. These stress effects
on lipid accumulation and TNF-α were abolished in SF rats (P < 0.05).
Conclusions: Fructose does not enhance stress effects on hepatic lipid and glucose metabolism but attenuates its
effects on hepatic lipid accumulation and inflammation, suggesting that, in female rats, AMPK activation prevails over
stress-induced effects.
PB  - Oxford University Press on behalf of the American Society of Nutrition
T2  - The Journal of Nutrition
T1  - Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats
IS  - 12
VL  - 151
DO  - 10.1093/jn/nxab294
SP  - 3661
EP  - 3670
ER  - 

@article{
author = "Kovačević, Sanja and Elaković, Ivana and Vojnović-Milutinović, Danijela and Nikolić-Kokić, Aleksandra and Blagojević, Duško and Matić, Gordana and Tappy, Luc and Đorđević, Ana and Brkljačić, Jelena",
year = "2021",
abstract = "Background: Both fructose consumption and chronic stress contribute to the development of metabolic disorders.
The consequences of such combination are not fully understood.
Objective: We investigated whether fructose supplementation and chronic stress synergistically disturb hepatic lipid
and glucose metabolism. The role of energy sensing, redox, and inflammatory status during development of metabolic
disturbances was investigated.
Methods: Female Wistar rats, aged 2.5 mo, were divided into 4 experimental groups: control (C) fed a standard diet
(commercial food and drinking water); fructose (F) fed the same food and 10% fructose solution; stress (S) fed the
standard diet and subjected to chronic unpredictable stress and, stress + fructose (SF) combining conditions F and
S as above. Stress included daily stressors: cold water forced swimming, physical restraint, cold room, wet bedding,
rocking, switching, or tilting cages. After 9 wk, hepatic enzymes and transcription factors involved in gluconeogenesis,
lipogenesis, fatty acid oxidation, antioxidative defence, energy sensing, and cytokines were assessed by qPCR, Western
blotting, and spectrophotometry and analyzed by 2-factor ANOVA.
Results: Fructose increased AMP-activated protein kinase (AMPK) phosphorylation (40%; P < 0.05) and the ratio of
inhibitory phosphorylation to total acetyl-CoA carboxylase (46%; P < 0.01), and decreased sterol regulatory element
binding protein 1c nuclear translocation by 30% (P < 0.05) in F and SF compared with C rats. Increased phosPck
(phoenolpyruvate carboxykinase) (85%) and G6pase (glucose-6-phosphatase) (55%) was observed in S rats (P < 0.05).
A 40% decrease in Apob (apolipoprotein B-100) and an increase in hepatic lipids (P < 0.05), together with a double
increase in TNF-α (P < 0.001), were observed in S rats, but without liver histopathological changes. These stress effects
on lipid accumulation and TNF-α were abolished in SF rats (P < 0.05).
Conclusions: Fructose does not enhance stress effects on hepatic lipid and glucose metabolism but attenuates its
effects on hepatic lipid accumulation and inflammation, suggesting that, in female rats, AMPK activation prevails over
stress-induced effects.",
publisher = "Oxford University Press on behalf of the American Society of Nutrition",
journal = "The Journal of Nutrition",
title = "Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats",
number = "12",
volume = "151",
doi = "10.1093/jn/nxab294",
pages = "3661-3670"
}

Kovačević, S., Elaković, I., Vojnović-Milutinović, D., Nikolić-Kokić, A., Blagojević, D., Matić, G., Tappy, L., Đorđević, A.,& Brkljačić, J.. (2021). Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats. in The Journal of Nutrition
Oxford University Press on behalf of the American Society of Nutrition., 151(12), 3661-3670.
https://doi.org/10.1093/jn/nxab294

Kovačević S, Elaković I, Vojnović-Milutinović D, Nikolić-Kokić A, Blagojević D, Matić G, Tappy L, Đorđević A, Brkljačić J. Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats. in The Journal of Nutrition. 2021;151(12):3661-3670.
doi:10.1093/jn/nxab294 .

Kovačević, Sanja, Elaković, Ivana, Vojnović-Milutinović, Danijela, Nikolić-Kokić, Aleksandra, Blagojević, Duško, Matić, Gordana, Tappy, Luc, Đorđević, Ana, Brkljačić, Jelena, "Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats" in The Journal of Nutrition, 151, no. 12 (2021):3661-3670,
https://doi.org/10.1093/jn/nxab294 . .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Vojnović-Milutinović, Danijela
AU  - Gligorovska, Ljupka
AU  - Bursać, Biljana
AU  - Elaković, Ivana
AU  - Đorđević, Ana
PY  - 2021
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4705
AB  - Introduction: Obesity and related metabolic disturbances are frequently related to
modern lifestyle and are characterized by excessive fructose intake. Visceral adipose
tissue (VAT) inflammation has a central role in the development of insulin resistance, type
2 diabetes (T2D), and metabolic syndrome. Since sex-related differences in susceptibility
and progression of metabolic disorders are not yet fully understood, our aim was to
examine inflammation and insulin signaling in VAT of fructose-fed female and male
adult rats.
Methods: We analyzed effects of 9-week 10% fructose-enriched diet on energy intake,
VATmass and histology, and systemic insulin sensitivity. VAT insulin signaling andmarkers
of VAT inflammation, and antioxidative defense status were also evaluated.
Results: The fructose diet had no effect on VAT mass and systemic insulin signaling
in the female and male rats, while it raised plasma uric acid, increased PPARg level in
the VAT, and initiated the development of a distinctive population of small adipocytes
in the females. Also, adipose tissue insulin resistance, evidenced by increased PTP1B
and insulin receptor substrate 1 (IRS1) inhibitory phosphorylation and decreased Akt
activity, was detected. In addition, fructose stimulated the nuclear accumulation of NFkB,
increased expression of proinflammatory cytokines (IL-1b, IL-6, and TNFα), and protein
level of macrophage marker F4/80, superoxide dismutase 1, and glutathione reductase.
In contrast to the females, the fructose diet had no effect on plasma uric acid and
VAT inflammation in the male rats, but less prominent alterations in VAT insulin signaling
were observed.
Conclusion: Even though dietary fructose did not elicit changes in energy intake and
led to obesity in the females, it initiated the proliferation of small-sized adipocytes capable
of storing fats further. In contrast to the males, this state of VAT was accompanied
with enhanced inflammation, which most likely contributed to the development of insulin
resistance. The observed distinction could possibly originate from sex-related differences
in uric acid metabolism. Our results suggest that VAT inflammation could precede obesity and start even before the measurable increase in VAT mass, making it a silent risk factor
for the development of T2D. Our results emphasize that adipose tissue dysfunction,
rather than its simple enlargement, could significantly contribute to the onset and
development of obesity and related metabolic disorders.
PB  - Lausanne: Frontiers Media SA
T2  - Frontiers in Nutrition
T1  - Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats
VL  - 8
DO  - 10.3389/fnut.2021.749328
SP  - 749328
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Vojnović-Milutinović, Danijela and Gligorovska, Ljupka and Bursać, Biljana and Elaković, Ivana and Đorđević, Ana",
year = "2021",
abstract = "Introduction: Obesity and related metabolic disturbances are frequently related to
modern lifestyle and are characterized by excessive fructose intake. Visceral adipose
tissue (VAT) inflammation has a central role in the development of insulin resistance, type
2 diabetes (T2D), and metabolic syndrome. Since sex-related differences in susceptibility
and progression of metabolic disorders are not yet fully understood, our aim was to
examine inflammation and insulin signaling in VAT of fructose-fed female and male
adult rats.
Methods: We analyzed effects of 9-week 10% fructose-enriched diet on energy intake,
VATmass and histology, and systemic insulin sensitivity. VAT insulin signaling andmarkers
of VAT inflammation, and antioxidative defense status were also evaluated.
Results: The fructose diet had no effect on VAT mass and systemic insulin signaling
in the female and male rats, while it raised plasma uric acid, increased PPARg level in
the VAT, and initiated the development of a distinctive population of small adipocytes
in the females. Also, adipose tissue insulin resistance, evidenced by increased PTP1B
and insulin receptor substrate 1 (IRS1) inhibitory phosphorylation and decreased Akt
activity, was detected. In addition, fructose stimulated the nuclear accumulation of NFkB,
increased expression of proinflammatory cytokines (IL-1b, IL-6, and TNFα), and protein
level of macrophage marker F4/80, superoxide dismutase 1, and glutathione reductase.
In contrast to the females, the fructose diet had no effect on plasma uric acid and
VAT inflammation in the male rats, but less prominent alterations in VAT insulin signaling
were observed.
Conclusion: Even though dietary fructose did not elicit changes in energy intake and
led to obesity in the females, it initiated the proliferation of small-sized adipocytes capable
of storing fats further. In contrast to the males, this state of VAT was accompanied
with enhanced inflammation, which most likely contributed to the development of insulin
resistance. The observed distinction could possibly originate from sex-related differences
in uric acid metabolism. Our results suggest that VAT inflammation could precede obesity and start even before the measurable increase in VAT mass, making it a silent risk factor
for the development of T2D. Our results emphasize that adipose tissue dysfunction,
rather than its simple enlargement, could significantly contribute to the onset and
development of obesity and related metabolic disorders.",
publisher = "Lausanne: Frontiers Media SA",
journal = "Frontiers in Nutrition",
title = "Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats",
volume = "8",
doi = "10.3389/fnut.2021.749328",
pages = "749328"
}

Kovačević, S., Brkljačić, J., Vojnović-Milutinović, D., Gligorovska, L., Bursać, B., Elaković, I.,& Đorđević, A.. (2021). Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats. in Frontiers in Nutrition
Lausanne: Frontiers Media SA., 8, 749328.
https://doi.org/10.3389/fnut.2021.749328

Kovačević S, Brkljačić J, Vojnović-Milutinović D, Gligorovska L, Bursać B, Elaković I, Đorđević A. Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats. in Frontiers in Nutrition. 2021;8:749328.
doi:10.3389/fnut.2021.749328 .

Kovačević, Sanja, Brkljačić, Jelena, Vojnović-Milutinović, Danijela, Gligorovska, Ljupka, Bursać, Biljana, Elaković, Ivana, Đorđević, Ana, "Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats" in Frontiers in Nutrition, 8 (2021):749328,
https://doi.org/10.3389/fnut.2021.749328 . .

TY  - JOUR
AU  - Elaković, Ivana
AU  - Kovačević, Sanja
AU  - Vojnović-Milutinović, Danijela
AU  - Nikolić-Kokić, Aleksandra
AU  - Glban, Alhadi M.
AU  - Spasić, Mihajlo
AU  - Tappy, Luc
AU  - Đorđević, Ana
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3983
AB  - The effects of early-life fructose consumption on hepatic signaling pathways and their relation to the development of metabolic disorders in later life are not fully understood. To investigate whether fructose over consumption at a young age induces alterations in glucocorticoid signaling that  might  contribute  to  development  of  metabolic  disturbances,  we  analysed  glucocorticoid receptor hormone-binding parameters and expression of its target genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) and lipid metabolism (lipin-1),as well as redox and inflammatory status in the liver of female rats subjected to a fructose-rich diet immediately after weaning.  The fructose diet increased hepatic corticosterone concentration,11β-hydroxysteroid  dehydrogenase  type  1  level,   glucocorticoid  receptor  protein  level  and hormone-binding activity, as well as lipin-1 level. The expression of glucose-6-phosphatase was reduced  in  fructose-fed  rats,  while  phosphoenolpyruvate  carboxykinase  remained  unaltered.The  fructose-rich  diet  increased  the  level  of  fructose  transporter  GLUT2,  while  the  expression of  fructolytic  enzymes  fructokinase  and  aldolase  B  remained  unaltered.   The  diet  also  affected pro-inflammatory pathways, but had no effect on the antioxidant defence system.  In conclusion, a fructose-rich diet applied immediately after weaning promoted lipogenesis and enhanced hepatic glucocorticoid signaling, possibly to protect against inflammatory damage, but without an effect on gluconeogenesis and antioxidant enzymes. Yet, prolonged treatment might ultimately lead to more pronounced metabolic disturbances.
PB  - Basel, Switzerland : Multidisciplinary Digital Publishing Institute (MDPI)
T2  - Nutrients
T1  - Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats
IS  - 11
VL  - 12
DO  - 10.3390/nu12113470
SP  - 3470
ER  - 

@article{
author = "Elaković, Ivana and Kovačević, Sanja and Vojnović-Milutinović, Danijela and Nikolić-Kokić, Aleksandra and Glban, Alhadi M. and Spasić, Mihajlo and Tappy, Luc and Đorđević, Ana and Matić, Gordana and Brkljačić, Jelena",
year = "2020",
abstract = "The effects of early-life fructose consumption on hepatic signaling pathways and their relation to the development of metabolic disorders in later life are not fully understood. To investigate whether fructose over consumption at a young age induces alterations in glucocorticoid signaling that  might  contribute  to  development  of  metabolic  disturbances,  we  analysed  glucocorticoid receptor hormone-binding parameters and expression of its target genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) and lipid metabolism (lipin-1),as well as redox and inflammatory status in the liver of female rats subjected to a fructose-rich diet immediately after weaning.  The fructose diet increased hepatic corticosterone concentration,11β-hydroxysteroid  dehydrogenase  type  1  level,   glucocorticoid  receptor  protein  level  and hormone-binding activity, as well as lipin-1 level. The expression of glucose-6-phosphatase was reduced  in  fructose-fed  rats,  while  phosphoenolpyruvate  carboxykinase  remained  unaltered.The  fructose-rich  diet  increased  the  level  of  fructose  transporter  GLUT2,  while  the  expression of  fructolytic  enzymes  fructokinase  and  aldolase  B  remained  unaltered.   The  diet  also  affected pro-inflammatory pathways, but had no effect on the antioxidant defence system.  In conclusion, a fructose-rich diet applied immediately after weaning promoted lipogenesis and enhanced hepatic glucocorticoid signaling, possibly to protect against inflammatory damage, but without an effect on gluconeogenesis and antioxidant enzymes. Yet, prolonged treatment might ultimately lead to more pronounced metabolic disturbances.",
publisher = "Basel, Switzerland : Multidisciplinary Digital Publishing Institute (MDPI)",
journal = "Nutrients",
title = "Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats",
number = "11",
volume = "12",
doi = "10.3390/nu12113470",
pages = "3470"
}

Elaković, I., Kovačević, S., Vojnović-Milutinović, D., Nikolić-Kokić, A., Glban, A. M., Spasić, M., Tappy, L., Đorđević, A., Matić, G.,& Brkljačić, J.. (2020). Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats. in Nutrients
Basel, Switzerland : Multidisciplinary Digital Publishing Institute (MDPI)., 12(11), 3470.
https://doi.org/10.3390/nu12113470

Elaković I, Kovačević S, Vojnović-Milutinović D, Nikolić-Kokić A, Glban AM, Spasić M, Tappy L, Đorđević A, Matić G, Brkljačić J. Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats. in Nutrients. 2020;12(11):3470.
doi:10.3390/nu12113470 .

Elaković, Ivana, Kovačević, Sanja, Vojnović-Milutinović, Danijela, Nikolić-Kokić, Aleksandra, Glban, Alhadi M., Spasić, Mihajlo, Tappy, Luc, Đorđević, Ana, Matić, Gordana, Brkljačić, Jelena, "Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats" in Nutrients, 12, no. 11 (2020):3470,
https://doi.org/10.3390/nu12113470 . .

TY  - CONF
AU  - Radovanović, Marina
AU  - Kovačević, Sanja
AU  - Elaković, Ivana
AU  - Vojnović-Milutinović, Danijela
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5252
AB  - The effects of early-life fructose consumption and their relation to metabolic diseases risk
in adulthood are not yet elucidated. This study explored the direct effects of a diet regime
characterized by fructose enrichment on glucocorticoid receptor signaling in the liver of
female rats immediately after weaning. 21 day-old female Wistar rats were subjected to a 9
week-long diet regime involving standard chow in combination with either the 10%
fructose solution or tap water. Glucocorticoid receptor hormone binding parameters,
intracellular distribution of this molecule as well as the expression of its target genes
involved in lipid metabolism (most notably Lipin-1) and glucose metabolism (PEPCK),
were measured. An increase in the hepatic glucocorticoid receptor hormone binding
activity as well as an elevated nuclear translocation of the receptor, in concert with the
increased protein levels of Lipin-1 were observed after fructose enriched diet. This was
preceeded by a hepatic elevation in Glut-2 fructose transporter expression. Fructose-
enriched diet starting immediately after weaning enhanced hepatic glucocorticoid signaling
in young female rats and promoted lypogenesis as evidenced not only by the lipin-1
increase but also by FAS, ACC and SCREBP-1 expression elevations contributing to
hypertriglyceridemia and the expansion of the visceral adipose tissue 1, with no effect on
the hepatic gluconeogenesis. These results imply that while most parameters remained
within physiological reactivity, prolonged treatment might ultimately lead to more
pronounced metabolic disturbances.
PB  - Belgrade: Faculty of Chemistry
C3  - The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia
T1  - Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5252
ER  - 

@conference{
author = "Radovanović, Marina and Kovačević, Sanja and Elaković, Ivana and Vojnović-Milutinović, Danijela and Matić, Gordana and Brkljačić, Jelena",
year = "2019",
abstract = "The effects of early-life fructose consumption and their relation to metabolic diseases risk
in adulthood are not yet elucidated. This study explored the direct effects of a diet regime
characterized by fructose enrichment on glucocorticoid receptor signaling in the liver of
female rats immediately after weaning. 21 day-old female Wistar rats were subjected to a 9
week-long diet regime involving standard chow in combination with either the 10%
fructose solution or tap water. Glucocorticoid receptor hormone binding parameters,
intracellular distribution of this molecule as well as the expression of its target genes
involved in lipid metabolism (most notably Lipin-1) and glucose metabolism (PEPCK),
were measured. An increase in the hepatic glucocorticoid receptor hormone binding
activity as well as an elevated nuclear translocation of the receptor, in concert with the
increased protein levels of Lipin-1 were observed after fructose enriched diet. This was
preceeded by a hepatic elevation in Glut-2 fructose transporter expression. Fructose-
enriched diet starting immediately after weaning enhanced hepatic glucocorticoid signaling
in young female rats and promoted lypogenesis as evidenced not only by the lipin-1
increase but also by FAS, ACC and SCREBP-1 expression elevations contributing to
hypertriglyceridemia and the expansion of the visceral adipose tissue 1, with no effect on
the hepatic gluconeogenesis. These results imply that while most parameters remained
within physiological reactivity, prolonged treatment might ultimately lead to more
pronounced metabolic disturbances.",
publisher = "Belgrade: Faculty of Chemistry",
journal = "The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia",
title = "Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5252"
}

Radovanović, M., Kovačević, S., Elaković, I., Vojnović-Milutinović, D., Matić, G.,& Brkljačić, J.. (2019). Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats. in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia
Belgrade: Faculty of Chemistry..
https://hdl.handle.net/21.15107/rcub_ibiss_5252

Radovanović M, Kovačević S, Elaković I, Vojnović-Milutinović D, Matić G, Brkljačić J. Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats. in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia. 2019;.
https://hdl.handle.net/21.15107/rcub_ibiss_5252 .

Radovanović, Marina, Kovačević, Sanja, Elaković, Ivana, Vojnović-Milutinović, Danijela, Matić, Gordana, Brkljačić, Jelena, "Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats" in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia (2019),
https://hdl.handle.net/21.15107/rcub_ibiss_5252 .

TY  - CONF
AU  - Kovačević, Sanja
AU  - Đorđević, Ana
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - https://www.faobmbkl2019.com/abstract-book
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3989
AB  - Modern diet, rich in refined sugars and sweeteners, led to dramatic increase in fructose intake especially in young population. Excessive fructose intake has been associated with growing rate of obesity, insulin resistance and development of metabolic syndrome, women being more prone than men. Chronic low-grade inflammation accompanies obesity and has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance. To elucidate whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) of young and adult female rats thus contributing to the development of obesity and insulin resistance. We investigated the effects of 9-week fructose-enriched diet applied immediately after weaning (young) or at the 2.5 months of age (adult) on nuclear factor κB (NF-κB) intracellular distribution, and on the expression of pro-inflammatory cytokines (IL-1β, IL-6 and TNFα) in female Wistar rats. Additionally, insulin signalling was analysed at the level of insulin receptor substrate-1 (IRS1), Akt kinase, and their activating and inhibitory phosphorylations. Fructose-enriched diet increased absolute and relative VAT mass in young female rats. There were no changes in VAT mass of adults after fructose diet, even though histological analysis revealed the presence of islets of smaller adipocytes, which indicated adipogenesis. Both young and adult female fructose-fed rats had increased nuclear accumulation of NF-κB and elevated expression of pro-inflammatory cytokines in the VAT. In adults, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of IRS-1. These changes were not observed in young female rats. The results suggest that fructose-enriched diet causes inflammation in VAT of both young and adult female rats. Our work supports the stand that VAT inflammation could represent one of the earliest metabolic perturbations upon fructose overconsumption, since it can occur even before the onset of obesity or insulin resistance. Additionally, only adults developed VAT insulin resistance, indicating age-dependent differences in insulin signalling system and its response to fructose overconsumption in female rats.
PB  - Malaysian Society for Biochemistry and Molecular Biology
PB  - Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB)
PB  - International Union of Biochemistry and Molecular Biology (IUBMB)
C3  - Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP)
T1  - Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats
SP  - 3
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3989
ER  - 

@conference{
author = "Kovačević, Sanja and Đorđević, Ana and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "Modern diet, rich in refined sugars and sweeteners, led to dramatic increase in fructose intake especially in young population. Excessive fructose intake has been associated with growing rate of obesity, insulin resistance and development of metabolic syndrome, women being more prone than men. Chronic low-grade inflammation accompanies obesity and has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance. To elucidate whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) of young and adult female rats thus contributing to the development of obesity and insulin resistance. We investigated the effects of 9-week fructose-enriched diet applied immediately after weaning (young) or at the 2.5 months of age (adult) on nuclear factor κB (NF-κB) intracellular distribution, and on the expression of pro-inflammatory cytokines (IL-1β, IL-6 and TNFα) in female Wistar rats. Additionally, insulin signalling was analysed at the level of insulin receptor substrate-1 (IRS1), Akt kinase, and their activating and inhibitory phosphorylations. Fructose-enriched diet increased absolute and relative VAT mass in young female rats. There were no changes in VAT mass of adults after fructose diet, even though histological analysis revealed the presence of islets of smaller adipocytes, which indicated adipogenesis. Both young and adult female fructose-fed rats had increased nuclear accumulation of NF-κB and elevated expression of pro-inflammatory cytokines in the VAT. In adults, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of IRS-1. These changes were not observed in young female rats. The results suggest that fructose-enriched diet causes inflammation in VAT of both young and adult female rats. Our work supports the stand that VAT inflammation could represent one of the earliest metabolic perturbations upon fructose overconsumption, since it can occur even before the onset of obesity or insulin resistance. Additionally, only adults developed VAT insulin resistance, indicating age-dependent differences in insulin signalling system and its response to fructose overconsumption in female rats.",
publisher = "Malaysian Society for Biochemistry and Molecular Biology, Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB), International Union of Biochemistry and Molecular Biology (IUBMB)",
journal = "Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP)",
title = "Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats",
pages = "3",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3989"
}

Kovačević, S., Đorđević, A., Matić, G.,& Elaković, I.. (2019). Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats. in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP)
Malaysian Society for Biochemistry and Molecular Biology., 3.
https://hdl.handle.net/21.15107/rcub_ibiss_3989

Kovačević S, Đorđević A, Matić G, Elaković I. Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats. in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP). 2019;:3.
https://hdl.handle.net/21.15107/rcub_ibiss_3989 .

Kovačević, Sanja, Đorđević, Ana, Matić, Gordana, Elaković, Ivana, "Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats" in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP) (2019):3,
https://hdl.handle.net/21.15107/rcub_ibiss_3989 .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - http://www.ncbi.nlm.nih.gov/pubmed/30572328
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3387
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3404
AB  - BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.
T2  - Neuroendocrinology
T1  - Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.
DO  - 10.1159/000496391
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.",
journal = "Neuroendocrinology",
title = "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.",
doi = "10.1159/000496391"
}

Kovačević, S., Brkljačić, J., Matić, G.,& Elaković, I.. (2019). Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology.
https://doi.org/10.1159/000496391

Kovačević S, Brkljačić J, Matić G, Elaković I. Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology. 2019;.
doi:10.1159/000496391 .

Kovačević, Sanja, Brkljačić, Jelena, Matić, Gordana, Elaković, Ivana, "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats." in Neuroendocrinology (2019),
https://doi.org/10.1159/000496391 . .

TY  - CONF
AU  - Kovačević, Sanja
AU  - Bursać, Biljana
AU  - Đorđević, Ana
AU  - Gligorovska, Ljupka
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3988
AB  - Background: Increased consumption of caloric food rich in fructose and daily exposure to unpredictable stress became hallmarks of modern lifestyle and have been associated with the development of metabolic syndrome, type2 diabetes and cardiovascular diseases1,2. Visceral  adipose  tissue  (VAT)  and  muscles are important centers of lipid and glucose metabolism and metabolic disturbances  in  these  organs  and  their crosstalk  could  vastly contribute to the development of metabolic diseases3,4. The  aim: To  elucidate  whether prolonged combination of fructose  over consumption and chronic stress disturbs lipid metabolism and insulin signaling in rat VAT and muscle. Methods: We  examined the  effects  of  9-week  fructose-enriched diet with  and  without exposure to unpredictable stress on expression of genes and level of proteins involved in lipid  uptake (lipoprotein lipase, fatty  acid  translocase  and fatty  acid transport  protein), de novo lipogenesis    (acetyl-CoA    carboxylase    and fatty    acid    synthase), lipolysis (hormone sensitive lipase and adipose   triglyceride   lipase)   and fatty   acids oxidation (carnitine  palmitoyltransferase  I)  in VAT  and muscle of  male  Wistar  rats.  Additionally, muscle  insulin  signaling  was  analyzed at the  level  of insulin receptor  substrate-1  (IRS1) and Akt kinase, and their activating and inhibitory phosphorylations. Results: Combination  of  fructose  overconsumption  and  stress increased plasma insulin and free fatty acids level, upregulated expression of both lipolytic and lipogenic genes in VAT and stimulated lipid uptake, lipolysis and β-oxidation in muscle. Furthermore, reduced protein  content  and  stimulatory  phosphorylation  of IRS1  and Akt  kinase, together  with unchanged inhibitory phosphorylation of IRS1 was observed in muscle. Conclusions: The  results show that the  combination  of fructose  over consumption and chronic stress disturbs lipid metabolism in VAT and muscle. Importantly, upregulated VAT lipolysis  elevates  plasma  free  fatty  acids, which  intensify their  influx  to  muscles  possibly leading to muscle insulin resistance detected in fructose fed stressed rats.
PB  - EMBO Press
C3  - EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain
T1  - Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats
SP  - 45
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3988
ER  - 

@conference{
author = "Kovačević, Sanja and Bursać, Biljana and Đorđević, Ana and Gligorovska, Ljupka and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "Background: Increased consumption of caloric food rich in fructose and daily exposure to unpredictable stress became hallmarks of modern lifestyle and have been associated with the development of metabolic syndrome, type2 diabetes and cardiovascular diseases1,2. Visceral  adipose  tissue  (VAT)  and  muscles are important centers of lipid and glucose metabolism and metabolic disturbances  in  these  organs  and  their crosstalk  could  vastly contribute to the development of metabolic diseases3,4. The  aim: To  elucidate  whether prolonged combination of fructose  over consumption and chronic stress disturbs lipid metabolism and insulin signaling in rat VAT and muscle. Methods: We  examined the  effects  of  9-week  fructose-enriched diet with  and  without exposure to unpredictable stress on expression of genes and level of proteins involved in lipid  uptake (lipoprotein lipase, fatty  acid  translocase  and fatty  acid transport  protein), de novo lipogenesis    (acetyl-CoA    carboxylase    and fatty    acid    synthase), lipolysis (hormone sensitive lipase and adipose   triglyceride   lipase)   and fatty   acids oxidation (carnitine  palmitoyltransferase  I)  in VAT  and muscle of  male  Wistar  rats.  Additionally, muscle  insulin  signaling  was  analyzed at the  level  of insulin receptor  substrate-1  (IRS1) and Akt kinase, and their activating and inhibitory phosphorylations. Results: Combination  of  fructose  overconsumption  and  stress increased plasma insulin and free fatty acids level, upregulated expression of both lipolytic and lipogenic genes in VAT and stimulated lipid uptake, lipolysis and β-oxidation in muscle. Furthermore, reduced protein  content  and  stimulatory  phosphorylation  of IRS1  and Akt  kinase, together  with unchanged inhibitory phosphorylation of IRS1 was observed in muscle. Conclusions: The  results show that the  combination  of fructose  over consumption and chronic stress disturbs lipid metabolism in VAT and muscle. Importantly, upregulated VAT lipolysis  elevates  plasma  free  fatty  acids, which  intensify their  influx  to  muscles  possibly leading to muscle insulin resistance detected in fructose fed stressed rats.",
publisher = "EMBO Press",
journal = "EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain",
title = "Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats",
pages = "45",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3988"
}

Kovačević, S., Bursać, B., Đorđević, A., Gligorovska, L., Matić, G.,& Elaković, I.. (2019). Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats. in EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain
EMBO Press., 45.
https://hdl.handle.net/21.15107/rcub_ibiss_3988

Kovačević S, Bursać B, Đorđević A, Gligorovska L, Matić G, Elaković I. Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats. in EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain. 2019;:45.
https://hdl.handle.net/21.15107/rcub_ibiss_3988 .

Kovačević, Sanja, Bursać, Biljana, Đorđević, Ana, Gligorovska, Ljupka, Matić, Gordana, Elaković, Ivana, "Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats" in EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain (2019):45,
https://hdl.handle.net/21.15107/rcub_ibiss_3988 .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - http://www.ncbi.nlm.nih.gov/pubmed/30572328
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3387
AB  - BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.
T2  - Neuroendocrinology
T1  - Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.
IS  - 4
VL  - 108
DO  - 10.1159/000496391
SP  - 278
EP  - 290
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.",
journal = "Neuroendocrinology",
title = "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.",
number = "4",
volume = "108",
doi = "10.1159/000496391",
pages = "278-290"
}

Kovačević, S., Brkljačić, J., Matić, G.,& Elaković, I.. (2019). Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology, 108(4), 278-290.
https://doi.org/10.1159/000496391

Kovačević S, Brkljačić J, Matić G, Elaković I. Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology. 2019;108(4):278-290.
doi:10.1159/000496391 .

Kovačević, Sanja, Brkljačić, Jelena, Matić, Gordana, Elaković, Ivana, "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats." in Neuroendocrinology, 108, no. 4 (2019):278-290,
https://doi.org/10.1159/000496391 . .

TY  - JOUR
AU  - Brkljačić, Jelena
AU  - Veličković, Nataša
AU  - Elaković, Ivana
AU  - Teofilović, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Đorđević, Ana
AU  - Matić, Gordana
PY  - 2019
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641900023N
UR  - http://www.serbiosoc.org.rs/arch/index.php/abs/article/view/4079
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3573
AB  - An increase in fructose consumption coincides with a rising incidence of metabolic disorders. Dietary fructose has been shown to affect hepatic lipid metabolism in a way that may lead to lipid deposition in the liver. In this study, we tested the hypothesis that the effects of fructose overconsumption on hepatic lipid metabolism differ between sexes. To that end we examined the effects of a high-fructose diet on the expression of key enzymes and transcription factors involved in the regulation of fatty acid oxidation and de novo lipogenesis in the liver of 12-week-old male and female Wistar rats. Immediately after weaning, the rats were subjected to a standard diet and 10% fructose solution or drinking water for 9 weeks. The fructose-enriched diet induced hypertriglyceridemia and increased hepatic de novo lipogenesis in both sexes, without lipid deposition in the liver. At the same time, visceral adiposity was observed only in female rats, while in males the treatment stimulated hepatic fatty acid oxidation. The fructose-enriched diet induced sex-specific effects on hepatic lipid metabolism in young rats. These results imply that male and female rats employ different strategies to cope with dietary fructose-related energy overload and to avoid lipid accumulation in the liver.
T2  - Archives of Biological Sciences
T1  - Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways
IS  - 3
VL  - 71
DO  - 10.2298/ABS190306023N
SP  - 417
EP  - 424
ER  - 

@article{
author = "Brkljačić, Jelena and Veličković, Nataša and Elaković, Ivana and Teofilović, Ana and Vojnović-Milutinović, Danijela and Đorđević, Ana and Matić, Gordana",
year = "2019",
abstract = "An increase in fructose consumption coincides with a rising incidence of metabolic disorders. Dietary fructose has been shown to affect hepatic lipid metabolism in a way that may lead to lipid deposition in the liver. In this study, we tested the hypothesis that the effects of fructose overconsumption on hepatic lipid metabolism differ between sexes. To that end we examined the effects of a high-fructose diet on the expression of key enzymes and transcription factors involved in the regulation of fatty acid oxidation and de novo lipogenesis in the liver of 12-week-old male and female Wistar rats. Immediately after weaning, the rats were subjected to a standard diet and 10% fructose solution or drinking water for 9 weeks. The fructose-enriched diet induced hypertriglyceridemia and increased hepatic de novo lipogenesis in both sexes, without lipid deposition in the liver. At the same time, visceral adiposity was observed only in female rats, while in males the treatment stimulated hepatic fatty acid oxidation. The fructose-enriched diet induced sex-specific effects on hepatic lipid metabolism in young rats. These results imply that male and female rats employ different strategies to cope with dietary fructose-related energy overload and to avoid lipid accumulation in the liver.",
journal = "Archives of Biological Sciences",
title = "Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways",
number = "3",
volume = "71",
doi = "10.2298/ABS190306023N",
pages = "417-424"
}

Brkljačić, J., Veličković, N., Elaković, I., Teofilović, A., Vojnović-Milutinović, D., Đorđević, A.,& Matić, G.. (2019). Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways. in Archives of Biological Sciences, 71(3), 417-424.
https://doi.org/10.2298/ABS190306023N

Brkljačić J, Veličković N, Elaković I, Teofilović A, Vojnović-Milutinović D, Đorđević A, Matić G. Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways. in Archives of Biological Sciences. 2019;71(3):417-424.
doi:10.2298/ABS190306023N .

Brkljačić, Jelena, Veličković, Nataša, Elaković, Ivana, Teofilović, Ana, Vojnović-Milutinović, Danijela, Đorđević, Ana, Matić, Gordana, "Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways" in Archives of Biological Sciences, 71, no. 3 (2019):417-424,
https://doi.org/10.2298/ABS190306023N . .

TY  - CONF
AU  - Veličković, Nataša
AU  - Teofilović, Ana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Bursać, Biljana
AU  - Brkljačić, Jelena
AU  - Elaković, Ivana
AU  - Kovačević, Sanja
AU  - Gligorovska, Ljupka
AU  - Radovanović, Marina
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5253
AB  - The aim: High fructose diet and chronic stress were both
linked with metabolic disturbances. Thus, we analyzed
their separate and combined effects on metabolic ho-
meostasis, with particular focus on hepatic lipogenesis
and gluconeogenesis.
Methods: Male Wistar rats were subjected to 9-week
20% fructose diet and/or 4-week chronic unpredict-
able stress. The following morphological and bio-
chemical parameters of lipid and glucose metabolism
were measured: body and liver mass, energy intake,
blood glucose and plasma insulin levels, free fatty ac-
ids (FFA), lactate, triglycerides (TG) and VLDL-TG, as
well as hepatic VLDL production rate, total hepatic TG
and palmitate and stearate percentage shares. Fur-
thermore, the expression of transcriptional regulators
and enzymes of hepatic de novo lipogenesis (DNL), li-
poprotein export and gluconeogenesis were analyzed.
Results: Although energy intake was increased after
fructose diet, body and liver mass remained unaltered.
Plasma TG were elevated in both fructose-fed groups,
whereas FFA were increased in the non-stressed fruc-
tose-fed group. Parameters of hepatic TG and VLDL
production and export were unaffected, except for the
hepatic palmitate production which was increased after
combined treatment. The increments of fractional DNL
and palmitate production accompanied the upregu-
lation of lipogenic enzymes, fatty acid sythase and
acetyl-CoA carboxylase, which was, interestingly, not
preceeded by the increase of their transcriptional reg-
ulators. In both fructose-fed groups blood glucose level
was increased, although hepatic gluconeogenesis
was unaffected.
Conclusion: Combined stress/fructose treatment is
more aggravating than separate treatments, since it
leads to an increase in hepatic de novo lipogenesis
and total hepatic TG palmitate, without concomitant
changes in VLDL production and export.
PB  - Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade
C3  - Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.
T1  - De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress
SP  - 18
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5253
ER  - 

@conference{
author = "Veličković, Nataša and Teofilović, Ana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Bursać, Biljana and Brkljačić, Jelena and Elaković, Ivana and Kovačević, Sanja and Gligorovska, Ljupka and Radovanović, Marina and Preitner, Frederic and Tappy, Luc and Matić, Gordana",
year = "2018",
abstract = "The aim: High fructose diet and chronic stress were both
linked with metabolic disturbances. Thus, we analyzed
their separate and combined effects on metabolic ho-
meostasis, with particular focus on hepatic lipogenesis
and gluconeogenesis.
Methods: Male Wistar rats were subjected to 9-week
20% fructose diet and/or 4-week chronic unpredict-
able stress. The following morphological and bio-
chemical parameters of lipid and glucose metabolism
were measured: body and liver mass, energy intake,
blood glucose and plasma insulin levels, free fatty ac-
ids (FFA), lactate, triglycerides (TG) and VLDL-TG, as
well as hepatic VLDL production rate, total hepatic TG
and palmitate and stearate percentage shares. Fur-
thermore, the expression of transcriptional regulators
and enzymes of hepatic de novo lipogenesis (DNL), li-
poprotein export and gluconeogenesis were analyzed.
Results: Although energy intake was increased after
fructose diet, body and liver mass remained unaltered.
Plasma TG were elevated in both fructose-fed groups,
whereas FFA were increased in the non-stressed fruc-
tose-fed group. Parameters of hepatic TG and VLDL
production and export were unaffected, except for the
hepatic palmitate production which was increased after
combined treatment. The increments of fractional DNL
and palmitate production accompanied the upregu-
lation of lipogenic enzymes, fatty acid sythase and
acetyl-CoA carboxylase, which was, interestingly, not
preceeded by the increase of their transcriptional reg-
ulators. In both fructose-fed groups blood glucose level
was increased, although hepatic gluconeogenesis
was unaffected.
Conclusion: Combined stress/fructose treatment is
more aggravating than separate treatments, since it
leads to an increase in hepatic de novo lipogenesis
and total hepatic TG palmitate, without concomitant
changes in VLDL production and export.",
publisher = "Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade",
journal = "Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.",
title = "De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress",
pages = "18",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5253"
}

Veličković, N., Teofilović, A., Đorđević, A., Vojnović-Milutinović, D., Bursać, B., Brkljačić, J., Elaković, I., Kovačević, S., Gligorovska, L., Radovanović, M., Preitner, F., Tappy, L.,& Matić, G.. (2018). De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress. in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.
Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade., 18.
https://hdl.handle.net/21.15107/rcub_ibiss_5253

Veličković N, Teofilović A, Đorđević A, Vojnović-Milutinović D, Bursać B, Brkljačić J, Elaković I, Kovačević S, Gligorovska L, Radovanović M, Preitner F, Tappy L, Matić G. De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress. in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.. 2018;:18.
https://hdl.handle.net/21.15107/rcub_ibiss_5253 .

Veličković, Nataša, Teofilović, Ana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Bursać, Biljana, Brkljačić, Jelena, Elaković, Ivana, Kovačević, Sanja, Gligorovska, Ljupka, Radovanović, Marina, Preitner, Frederic, Tappy, Luc, Matić, Gordana, "De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress" in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia. (2018):18,
https://hdl.handle.net/21.15107/rcub_ibiss_5253 .

TY  - CONF
AU  - Kovačević, Sanja
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2018
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3986
AB  - Introduction 
Increased fructose consumption, mainly through sweetened beverages, coincides with growing rate of obesity, women being more prone than men. Chronic low-grade inflammation has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance.
The aim 
We investigated whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) and hypothalamus of female rats contributing to development of obesity and insulin resistance.
Methods 
Using qPCR and Western blot, we examined the effects of 9-week fructose-enriched diet on inflammatory status, insulin and leptin signaling in the VAT and hypothalamus, as well as on the expression of orexigenic and anorexigenic neuropeptides in the hypothalamus.
Results 
Fructose-fed rats had increased nuclear accumulation of nuclear factor κB (NF-κB) and elevated expression of pro-inflammatory cytokines (IL-1β, IL6, and TNFα), as well as increased protein level of macrophage-specific marker F4/80 in the VAT. In the same tissue, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1). There were no changes in VAT mass, nor in inflammatory markers, insulin and leptin signaling (leptin receptor and SOCS3 expression) and appetite regulation (NPY, AgRP, POMC and CART) in the hypothalamus.
Conclusions 
The results suggest that fructose overconsumption causes alterations in pro-inflammatory markers and reduces insulin signaling in the VAT of female rats. These alterations could be one of the first consequences of fructose overconsumption, since they were detected in the absence of obesity, and hypothalamic inflammation and insulin and leptin resistance.
PB  - Belgrade: Institute for Biological Research “Siniša Stanković”
C3  - Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging
T1  - Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats
SP  - 34
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3986
ER  - 

@conference{
editor = "Đorđević, Ana",
author = "Kovačević, Sanja and Matić, Gordana and Elaković, Ivana",
year = "2018",
abstract = "Introduction 
Increased fructose consumption, mainly through sweetened beverages, coincides with growing rate of obesity, women being more prone than men. Chronic low-grade inflammation has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance.
The aim 
We investigated whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) and hypothalamus of female rats contributing to development of obesity and insulin resistance.
Methods 
Using qPCR and Western blot, we examined the effects of 9-week fructose-enriched diet on inflammatory status, insulin and leptin signaling in the VAT and hypothalamus, as well as on the expression of orexigenic and anorexigenic neuropeptides in the hypothalamus.
Results 
Fructose-fed rats had increased nuclear accumulation of nuclear factor κB (NF-κB) and elevated expression of pro-inflammatory cytokines (IL-1β, IL6, and TNFα), as well as increased protein level of macrophage-specific marker F4/80 in the VAT. In the same tissue, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1). There were no changes in VAT mass, nor in inflammatory markers, insulin and leptin signaling (leptin receptor and SOCS3 expression) and appetite regulation (NPY, AgRP, POMC and CART) in the hypothalamus.
Conclusions 
The results suggest that fructose overconsumption causes alterations in pro-inflammatory markers and reduces insulin signaling in the VAT of female rats. These alterations could be one of the first consequences of fructose overconsumption, since they were detected in the absence of obesity, and hypothalamic inflammation and insulin and leptin resistance.",
publisher = "Belgrade: Institute for Biological Research “Siniša Stanković”",
journal = "Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging",
title = "Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats",
pages = "34",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3986"
}

Đorđević, A., Kovačević, S., Matić, G.,& Elaković, I.. (2018). Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats. in Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging
Belgrade: Institute for Biological Research “Siniša Stanković”., 34.
https://hdl.handle.net/21.15107/rcub_ibiss_3986

Đorđević A, Kovačević S, Matić G, Elaković I. Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats. in Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging. 2018;:34.
https://hdl.handle.net/21.15107/rcub_ibiss_3986 .

Đorđević, Ana, Kovačević, Sanja, Matić, Gordana, Elaković, Ivana, "Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats" in Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging (2018):34,
https://hdl.handle.net/21.15107/rcub_ibiss_3986 .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5148
AB  - Purpose Daily exposure to stress and excessive fruc-
tose intake coincides with the growing rate of obesity and
related disorders, to which women are more prone than
men. Glucocorticoids, the main regulators of energy bal-
ance and response to stress, have been associated with the
development of metabolic disturbances. The aim of the pre-
sent study was to examine the effects of fructose overcon-
sumption and/or chronic stress on glucocorticoid signaliza-
tion and lipid metabolism in female rat adipose tissue.
Methods We examined the effects of fructose-enriched
diet and chronic unpredictable stress, separately and in
combination, on glucocorticoid signaling in terms of
11β-hydroxysteroid dehydrogenase 1 (HSD1)-catalyzed
corticosterone regeneration, glucocorticoid receptor (GR)
intracellular distribution, hormone binding and transcrip-
tional regulation of genes involved in lipolysis (hormone-
sensitive lipase) and lipogenesis (lipoprotein lipase,
acetyl-CoA carboxylase, fatty acid synthase and phospho-
enolpyruvate carboxykinase) in the visceral adipose tis-
sue (VAT) of adult female rats. Additionally, the nuclear
level of the peroxisomal proliferator-activated receptor γ
(PPARγ) was analyzed.
Results The combination of stress and fructose-enriched
diet led to an elevation in HSD1 expression and intracel-
lular corticosterone concentration, whereas GR nuclear
accumulation was enhanced after separate treatments. Fur-
thermore, fructose was shown to induce the expression of
all examined lipogenic genes and nuclear accumulation
of PPARγ, thereby stimulating adipogenesis, while stress
upregulated HSL, reducing the adipose tissue mass regard-
less of fructose consumption.
Conclusions Prolonged overconsumption of fructose and
chronic exposure to stress promote opposite effects on lipid
metabolism in the VAT of adult female rats and suggest that
these effects could be mediated by glucocorticoids
PB  - Heidelberg: Springer
T2  - European Journal of Nutrition
T1  - Fructose and stress induce opposite effects on lipid metabolism in the visceral adipose tissue of adult female rats through glucocorticoid action
IS  - 6
VL  - 56
DO  - 10.1007/s00394-016-1251-8
SP  - 2115
EP  - 2128
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Matić, Gordana and Elaković, Ivana",
year = "2017",
abstract = "Purpose Daily exposure to stress and excessive fruc-
tose intake coincides with the growing rate of obesity and
related disorders, to which women are more prone than
men. Glucocorticoids, the main regulators of energy bal-
ance and response to stress, have been associated with the
development of metabolic disturbances. The aim of the pre-
sent study was to examine the effects of fructose overcon-
sumption and/or chronic stress on glucocorticoid signaliza-
tion and lipid metabolism in female rat adipose tissue.
Methods We examined the effects of fructose-enriched
diet and chronic unpredictable stress, separately and in
combination, on glucocorticoid signaling in terms of
11β-hydroxysteroid dehydrogenase 1 (HSD1)-catalyzed
corticosterone regeneration, glucocorticoid receptor (GR)
intracellular distribution, hormone binding and transcrip-
tional regulation of genes involved in lipolysis (hormone-
sensitive lipase) and lipogenesis (lipoprotein lipase,
acetyl-CoA carboxylase, fatty acid synthase and phospho-
enolpyruvate carboxykinase) in the visceral adipose tis-
sue (VAT) of adult female rats. Additionally, the nuclear
level of the peroxisomal proliferator-activated receptor γ
(PPARγ) was analyzed.
Results The combination of stress and fructose-enriched
diet led to an elevation in HSD1 expression and intracel-
lular corticosterone concentration, whereas GR nuclear
accumulation was enhanced after separate treatments. Fur-
thermore, fructose was shown to induce the expression of
all examined lipogenic genes and nuclear accumulation
of PPARγ, thereby stimulating adipogenesis, while stress
upregulated HSL, reducing the adipose tissue mass regard-
less of fructose consumption.
Conclusions Prolonged overconsumption of fructose and
chronic exposure to stress promote opposite effects on lipid
metabolism in the VAT of adult female rats and suggest that
these effects could be mediated by glucocorticoids",
publisher = "Heidelberg: Springer",
journal = "European Journal of Nutrition",
title = "Fructose and stress induce opposite effects on lipid metabolism in the visceral adipose tissue of adult female rats through glucocorticoid action",
number = "6",
volume = "56",
doi = "10.1007/s00394-016-1251-8",
pages = "2115-2128"
}

Kovačević, S., Brkljačić, J., Matić, G.,& Elaković, I.. (2017). Fructose and stress induce opposite effects on lipid metabolism in the visceral adipose tissue of adult female rats through glucocorticoid action. in European Journal of Nutrition
Heidelberg: Springer., 56(6), 2115-2128.
https://doi.org/10.1007/s00394-016-1251-8

Kovačević S, Brkljačić J, Matić G, Elaković I. Fructose and stress induce opposite effects on lipid metabolism in the visceral adipose tissue of adult female rats through glucocorticoid action. in European Journal of Nutrition. 2017;56(6):2115-2128.
doi:10.1007/s00394-016-1251-8 .

Kovačević, Sanja, Brkljačić, Jelena, Matić, Gordana, Elaković, Ivana, "Fructose and stress induce opposite effects on lipid metabolism in the visceral adipose tissue of adult female rats through glucocorticoid action" in European Journal of Nutrition, 56, no. 6 (2017):2115-2128,
https://doi.org/10.1007/s00394-016-1251-8 . .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2017
UR  - http://link.springer.com/10.1007/s00394-015-1065-0
UR  - http://www.ncbi.nlm.nih.gov/pubmed/26433940
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2917
AB  - PURPOSE The consumption of refined, fructose-enriched food continuously increases and has been linked to development of obesity, especially in young population. Low-grade inflammation and increased oxidative stress have been implicated in the pathogenesis of obesity-related disorders including type 2 diabetes. In this study, we examined alterations in inflammation and antioxidative defense system in the visceral adipose tissue (VAT) of fructose-fed young female rats, and related them to changes in adiposity and insulin sensitivity. METHODS We examined the effects of 9-week fructose-enriched diet applied immediately after weaning on nuclear factor κB (NF-κB) intracellular distribution, and on the expression of pro-inflammatory cytokines (IL-1β and TNFα) and key antioxidative enzymes in the VAT of female rats. Insulin signaling in the VAT was evaluated at the level of insulin receptor substrate-1 (IRS-1) protein and its inhibitory phosphorylation on Ser307. RESULTS Fructose-fed rats had increased VAT mass along with increased NF-κB nuclear accumulation and elevated IL-1β, but not TNFα expression. The protein levels of antioxidative defense enzymes, mitochondrial manganese superoxide dismutase 2, and glutathione peroxidase, were reduced, while the protein content of IRS-1 and its inhibitory phosphorylation were not altered by fructose diet. CONCLUSIONS The results suggest that fructose overconsumption-related alterations in pro-inflammatory markers and antioxidative capacity in the VAT of young female rats can be implicated in the development of adiposity, but do not affect inhibitory phosphorylation of IRS-1.
T2  - European journal of nutrition
T2  - European Journal of Nutrition
T1  - Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats.
IS  - 1
VL  - 56
DO  - 10.1007/s00394-015-1065-0
SP  - 151
EP  - 160
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Matić, Gordana and Elaković, Ivana",
year = "2017",
abstract = "PURPOSE The consumption of refined, fructose-enriched food continuously increases and has been linked to development of obesity, especially in young population. Low-grade inflammation and increased oxidative stress have been implicated in the pathogenesis of obesity-related disorders including type 2 diabetes. In this study, we examined alterations in inflammation and antioxidative defense system in the visceral adipose tissue (VAT) of fructose-fed young female rats, and related them to changes in adiposity and insulin sensitivity. METHODS We examined the effects of 9-week fructose-enriched diet applied immediately after weaning on nuclear factor κB (NF-κB) intracellular distribution, and on the expression of pro-inflammatory cytokines (IL-1β and TNFα) and key antioxidative enzymes in the VAT of female rats. Insulin signaling in the VAT was evaluated at the level of insulin receptor substrate-1 (IRS-1) protein and its inhibitory phosphorylation on Ser307. RESULTS Fructose-fed rats had increased VAT mass along with increased NF-κB nuclear accumulation and elevated IL-1β, but not TNFα expression. The protein levels of antioxidative defense enzymes, mitochondrial manganese superoxide dismutase 2, and glutathione peroxidase, were reduced, while the protein content of IRS-1 and its inhibitory phosphorylation were not altered by fructose diet. CONCLUSIONS The results suggest that fructose overconsumption-related alterations in pro-inflammatory markers and antioxidative capacity in the VAT of young female rats can be implicated in the development of adiposity, but do not affect inhibitory phosphorylation of IRS-1.",
journal = "European journal of nutrition, European Journal of Nutrition",
title = "Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats.",
number = "1",
volume = "56",
doi = "10.1007/s00394-015-1065-0",
pages = "151-160"
}

Kovačević, S., Brkljačić, J., Matić, G.,& Elaković, I.. (2017). Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats.. in European journal of nutrition, 56(1), 151-160.
https://doi.org/10.1007/s00394-015-1065-0

Kovačević S, Brkljačić J, Matić G, Elaković I. Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats.. in European journal of nutrition. 2017;56(1):151-160.
doi:10.1007/s00394-015-1065-0 .

Kovačević, Sanja, Brkljačić, Jelena, Matić, Gordana, Elaković, Ivana, "Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats." in European journal of nutrition, 56, no. 1 (2017):151-160,
https://doi.org/10.1007/s00394-015-1065-0 . .

TY  - CHAP
AU  - Matić, Gordana
AU  - Vojnović-Milutinović, Danijela
AU  - Elaković, Ivana
AU  - Brkljačić, Jelena
AU  - Savić, Danka
PY  - 2016
UR  - http://link.springer.com/10.1007/978-3-319-08359-9_3
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2628
AB  - This chapter summarizes current research on glucocorticoid receptor (GR) functional alterations associated with trauma exposure, posttraumatic stress disorder (PTSD) psychopathology, and resilience and vulnerability to PTSD. Special attention is paid to hormone-binding activity of the receptor, the level of its expression, its ratio to mineralocorticoid receptor (MR), and the interactions of corticosteroid receptors with heat shock protein chaperones, Hsp90 and Hsp70. Determinations of GR number (Bmax) and assessments of lymphocyte sensitivity to glucocorticoids in trauma-exposed individuals with and without PTSD have yielded rather inconsistent results. The contribution of most other factors determining tissue responsiveness to glucocorticoid hormones to PTSD pathophysiology is currently under investigation. Thus, increased GR protein level in peripheral lymphocytes from current and lifetime PTSD patients in comparison to trauma-exposed non-PTSD individuals (trauma controls) appeared to be a possible correlate of vulnerability to PTSD. Besides, PTSD patients displayed the lowest and trauma controls the highest fractional occupancy of the GR, suggesting that the receptor redox status may be a factor contributing to vulnerability/resilience to PTSD. Estimates of the GR hormone-binding potency (Bmax/KD ratio) and of strength of correlation between Bmax and KD pointed to deterioration of glucocorticoid signaling in the lymphocytes as a characteristic of PTSD patients. Lymphocyte MR protein level, MR/GR ratio, and Hsp90 and Hsp70 levels were found to be unaffected by traumatic events and past or current PTSD symptoms. However, the association of GR and Hsp90 expression levels appeared as a candidate marker of trauma exposure, while that of MR and Hsp70 levels of vulnerability to PTSD.
PB  - Springer International Publishing
T2  - Comprehensive Guide to Post-Traumatic Stress Disorders
T1  - Level of Expression and Functional Properties of Lymphocyte Corticosteroid Receptors as Biological Correlates of PTSD, Trauma-Exposure, or Resilience to PTSD
DO  - 10.1007/978-3-319-08359-9_3
SP  - 961
EP  - 978
ER  - 

@inbook{
editor = "Martin, Colin R., Preedy, Victor R., Patel, Vinood B.",
author = "Matić, Gordana and Vojnović-Milutinović, Danijela and Elaković, Ivana and Brkljačić, Jelena and Savić, Danka",
year = "2016",
abstract = "This chapter summarizes current research on glucocorticoid receptor (GR) functional alterations associated with trauma exposure, posttraumatic stress disorder (PTSD) psychopathology, and resilience and vulnerability to PTSD. Special attention is paid to hormone-binding activity of the receptor, the level of its expression, its ratio to mineralocorticoid receptor (MR), and the interactions of corticosteroid receptors with heat shock protein chaperones, Hsp90 and Hsp70. Determinations of GR number (Bmax) and assessments of lymphocyte sensitivity to glucocorticoids in trauma-exposed individuals with and without PTSD have yielded rather inconsistent results. The contribution of most other factors determining tissue responsiveness to glucocorticoid hormones to PTSD pathophysiology is currently under investigation. Thus, increased GR protein level in peripheral lymphocytes from current and lifetime PTSD patients in comparison to trauma-exposed non-PTSD individuals (trauma controls) appeared to be a possible correlate of vulnerability to PTSD. Besides, PTSD patients displayed the lowest and trauma controls the highest fractional occupancy of the GR, suggesting that the receptor redox status may be a factor contributing to vulnerability/resilience to PTSD. Estimates of the GR hormone-binding potency (Bmax/KD ratio) and of strength of correlation between Bmax and KD pointed to deterioration of glucocorticoid signaling in the lymphocytes as a characteristic of PTSD patients. Lymphocyte MR protein level, MR/GR ratio, and Hsp90 and Hsp70 levels were found to be unaffected by traumatic events and past or current PTSD symptoms. However, the association of GR and Hsp90 expression levels appeared as a candidate marker of trauma exposure, while that of MR and Hsp70 levels of vulnerability to PTSD.",
publisher = "Springer International Publishing",
journal = "Comprehensive Guide to Post-Traumatic Stress Disorders",
booktitle = "Level of Expression and Functional Properties of Lymphocyte Corticosteroid Receptors as Biological Correlates of PTSD, Trauma-Exposure, or Resilience to PTSD",
doi = "10.1007/978-3-319-08359-9_3",
pages = "961-978"
}

Martin, C. R., Preedy, V. R., Patel, V. B., Matić, G., Vojnović-Milutinović, D., Elaković, I., Brkljačić, J.,& Savić, D.. (2016). Level of Expression and Functional Properties of Lymphocyte Corticosteroid Receptors as Biological Correlates of PTSD, Trauma-Exposure, or Resilience to PTSD. in Comprehensive Guide to Post-Traumatic Stress Disorders
Springer International Publishing., 961-978.
https://doi.org/10.1007/978-3-319-08359-9_3

Martin CR, Preedy VR, Patel VB, Matić G, Vojnović-Milutinović D, Elaković I, Brkljačić J, Savić D. Level of Expression and Functional Properties of Lymphocyte Corticosteroid Receptors as Biological Correlates of PTSD, Trauma-Exposure, or Resilience to PTSD. in Comprehensive Guide to Post-Traumatic Stress Disorders. 2016;:961-978.
doi:10.1007/978-3-319-08359-9_3 .

Martin, Colin R., Preedy, Victor R., Patel, Vinood B., Matić, Gordana, Vojnović-Milutinović, Danijela, Elaković, Ivana, Brkljačić, Jelena, Savić, Danka, "Level of Expression and Functional Properties of Lymphocyte Corticosteroid Receptors as Biological Correlates of PTSD, Trauma-Exposure, or Resilience to PTSD" in Comprehensive Guide to Post-Traumatic Stress Disorders (2016):961-978,
https://doi.org/10.1007/978-3-319-08359-9_3 . .

TY  - JOUR
AU  - Vojnović-Milutinović, Danijela
AU  - Radovanović, Marina
AU  - Dinic, Jovana
AU  - Đorđević, Ana
AU  - Velickovic, Natasa
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2273
AB  - Alterations in leptin and glucocorticoid signaling pathways in the
   hypothalamus of male and female rats subjected to a fructose-enriched
   diet were studied. The level of expression of the key components of the
   leptin signaling pathway (neuropeptide Y /NPY/ and suppressor of
   cytokine signaling 3 /SOCS3/), and the glucocorticoid signaling pathway
   (glucocorticoid receptor /GR/, 11 beta-hydroxysteroid dehydrogenase type
   1 /11 beta HSD1/ and hexose-6-phosphate dehydrogenase /H6PDH/) did not
   differ between fructose-fed rats and control animals of both genders.
   However, in females, a fructose-enriched diet provoked increases in the
   adiposity index, plasma leptin and triglyceride concentrations, and
   displayed a tendency to decrease the leptin receptor (ObRb) protein and
   mRNA levels. In male rats, the fructose diet caused elevations in plasma
   non-esterified fatty acids and triglycerides, as well as in both plasma
   and hypothalamic leptin concentrations. Our results suggest that a
   fructose-enriched diet can induce hyperleptinemia in both female and
   male rats, but with a more pronounced effect on hypothalamic leptin
   sensitivity in females, probably contributing to the observed
   development of visceral adiposity.
T2  - Archives of Biological Sciences
T1  - Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats
IS  - 2
VL  - 66
DO  - 10.2298/ABS1402829M
SP  - 829
EP  - 839
ER  - 

@article{
author = "Vojnović-Milutinović, Danijela and Radovanović, Marina and Dinic, Jovana and Đorđević, Ana and Velickovic, Natasa and Elaković, Ivana and Matić, Gordana and Brkljačić, Jelena",
year = "2014",
abstract = "Alterations in leptin and glucocorticoid signaling pathways in the
   hypothalamus of male and female rats subjected to a fructose-enriched
   diet were studied. The level of expression of the key components of the
   leptin signaling pathway (neuropeptide Y /NPY/ and suppressor of
   cytokine signaling 3 /SOCS3/), and the glucocorticoid signaling pathway
   (glucocorticoid receptor /GR/, 11 beta-hydroxysteroid dehydrogenase type
   1 /11 beta HSD1/ and hexose-6-phosphate dehydrogenase /H6PDH/) did not
   differ between fructose-fed rats and control animals of both genders.
   However, in females, a fructose-enriched diet provoked increases in the
   adiposity index, plasma leptin and triglyceride concentrations, and
   displayed a tendency to decrease the leptin receptor (ObRb) protein and
   mRNA levels. In male rats, the fructose diet caused elevations in plasma
   non-esterified fatty acids and triglycerides, as well as in both plasma
   and hypothalamic leptin concentrations. Our results suggest that a
   fructose-enriched diet can induce hyperleptinemia in both female and
   male rats, but with a more pronounced effect on hypothalamic leptin
   sensitivity in females, probably contributing to the observed
   development of visceral adiposity.",
journal = "Archives of Biological Sciences",
title = "Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats",
number = "2",
volume = "66",
doi = "10.2298/ABS1402829M",
pages = "829-839"
}

Vojnović-Milutinović, D., Radovanović, M., Dinic, J., Đorđević, A., Velickovic, N., Elaković, I., Matić, G.,& Brkljačić, J.. (2014). Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats. in Archives of Biological Sciences, 66(2), 829-839.
https://doi.org/10.2298/ABS1402829M

Vojnović-Milutinović D, Radovanović M, Dinic J, Đorđević A, Velickovic N, Elaković I, Matić G, Brkljačić J. Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats. in Archives of Biological Sciences. 2014;66(2):829-839.
doi:10.2298/ABS1402829M .

Vojnović-Milutinović, Danijela, Radovanović, Marina, Dinic, Jovana, Đorđević, Ana, Velickovic, Natasa, Elaković, Ivana, Matić, Gordana, Brkljačić, Jelena, "Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats" in Archives of Biological Sciences, 66, no. 2 (2014):829-839,
https://doi.org/10.2298/ABS1402829M . .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2167
AB  - Excessive fructose intake coincides with the growing rate of obesity and
   metabolic syndrome, with women being more prone to these disorders than
   men. Findings that detrimental effects of fructose might be mediated by
   glucocorticoid regeneration in adipose tissue only indirectly implicated
   glucocorticoid receptor (GR) in the phenomenon. The aim of the present
   study was to elucidate whether fructose overconsumption induces
   derangements in GR expression and function that might be associated with
   fructose-induced adiposity in females.
   We examined effects of fructose-enriched diet on GR expression and
   function in visceral adipose tissue of female rats. Additionally, we
   analyzed the expression of genes involved in glucocorticoid prereceptor
   metabolism {[}11 beta-hydroxysteroid dehydrogenase type 1 (11 beta HSD1)
   and hexose-6-phosphate dehydrogenase], lipolysis (hormone-sensitive
   lipase) and lipogenesis (sterol regulatory element binding protein 1 and
   peroxisomal proliferator-activated receptor gamma).
   Fructose-fed rats had elevated energy intake that resulted in visceral
   adiposity, as indicated by increased visceral adipose tissue mass and
   its share in the whole-body weight. GR hormone binding capacity and
   affinity, as well as the expression of GR gene at both mRNA and protein
   levels were reduced in visceral adipose tissue of the rats on fructose
   diet. The glucocorticoid prereceptor metabolism was stimulated, as
   evidenced by elevated tissue corticosterone, while the key regulators of
   lipolysis and lipogenesis remained unaffected by fructose diet.
   The results suggest that the 11 beta HSD1-mediated elevation of
   intracellular corticosterone may induce GR downregulation, which may be
   associated with failure of GR to stimulate lipolysis in fructose-fed
   female rats.
T2  - European Journal of Nutrition
T1  - Dietary fructose-related adiposity and glucocorticoid receptor function
 in visceral adipose tissue of female rats
IS  - 6
VL  - 53
DO  - 10.1007/s00394-013-0644-1
SP  - 1409
EP  - 1420
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Matić, Gordana and Elaković, Ivana",
year = "2014",
abstract = "Excessive fructose intake coincides with the growing rate of obesity and
   metabolic syndrome, with women being more prone to these disorders than
   men. Findings that detrimental effects of fructose might be mediated by
   glucocorticoid regeneration in adipose tissue only indirectly implicated
   glucocorticoid receptor (GR) in the phenomenon. The aim of the present
   study was to elucidate whether fructose overconsumption induces
   derangements in GR expression and function that might be associated with
   fructose-induced adiposity in females.
   We examined effects of fructose-enriched diet on GR expression and
   function in visceral adipose tissue of female rats. Additionally, we
   analyzed the expression of genes involved in glucocorticoid prereceptor
   metabolism {[}11 beta-hydroxysteroid dehydrogenase type 1 (11 beta HSD1)
   and hexose-6-phosphate dehydrogenase], lipolysis (hormone-sensitive
   lipase) and lipogenesis (sterol regulatory element binding protein 1 and
   peroxisomal proliferator-activated receptor gamma).
   Fructose-fed rats had elevated energy intake that resulted in visceral
   adiposity, as indicated by increased visceral adipose tissue mass and
   its share in the whole-body weight. GR hormone binding capacity and
   affinity, as well as the expression of GR gene at both mRNA and protein
   levels were reduced in visceral adipose tissue of the rats on fructose
   diet. The glucocorticoid prereceptor metabolism was stimulated, as
   evidenced by elevated tissue corticosterone, while the key regulators of
   lipolysis and lipogenesis remained unaffected by fructose diet.
   The results suggest that the 11 beta HSD1-mediated elevation of
   intracellular corticosterone may induce GR downregulation, which may be
   associated with failure of GR to stimulate lipolysis in fructose-fed
   female rats.",
journal = "European Journal of Nutrition",
title = "Dietary fructose-related adiposity and glucocorticoid receptor function
 in visceral adipose tissue of female rats",
number = "6",
volume = "53",
doi = "10.1007/s00394-013-0644-1",
pages = "1409-1420"
}

Kovačević, S., Brkljačić, J., Matić, G.,& Elaković, I.. (2014). Dietary fructose-related adiposity and glucocorticoid receptor function
 in visceral adipose tissue of female rats. in European Journal of Nutrition, 53(6), 1409-1420.
https://doi.org/10.1007/s00394-013-0644-1

Kovačević S, Brkljačić J, Matić G, Elaković I. Dietary fructose-related adiposity and glucocorticoid receptor function
 in visceral adipose tissue of female rats. in European Journal of Nutrition. 2014;53(6):1409-1420.
doi:10.1007/s00394-013-0644-1 .

Kovačević, Sanja, Brkljačić, Jelena, Matić, Gordana, Elaković, Ivana, "Dietary fructose-related adiposity and glucocorticoid receptor function
 in visceral adipose tissue of female rats" in European Journal of Nutrition, 53, no. 6 (2014):1409-1420,
https://doi.org/10.1007/s00394-013-0644-1 . .

TY  - JOUR
AU  - Matić, Gordana
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Elaković, Ivana
AU  - Manitašević Jovanović, Sanja
AU  - Elzaedi, Younis Mouftah
AU  - Perisic, Tatjana
AU  - Dunderski, Jadranka
AU  - Damjanovic, Svetozar
AU  - Knezevic, Goran
AU  - Spiric, Zeljko
AU  - Vermetten, Eric
AU  - Savic, Danka
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2244
AB  - Alterations in the number and functional status of mineralocorticoid
   (MR) and glucocorticoid receptors (GR) may contribute to vulnerability
   to posttraumatic stress disorder (PTSD). Corticosteroid receptors are
   chaperoned by heat shock proteins Hsp90 and Hsp70. We examined relations
   between corticosteroid receptor and heat shock protein expression
   levels, and related them with war trauma exposure, PTSD and resilience
   to PTSD. Relative levels of MR. Hsp90 and Hsp70 were determined by
   immunoblotting in lymphocytes from war trauma-exposed men with current
   PTSD (current PTSD group, n=113), with lifetime PTSD (life-time PTSD
   group, n=61) and without PTSD (trauma control group, n=88), and from
   non-traumatized healthy controls (healthy control group, n=85).
   Between-group differences in MR, Hsp90 and Hsp70 levels and in MR/GR
   ratio were not observed. The level of MR was correlated with both Hsp90
   and Hsp70 levels in trauma control and healthy control groups. On the
   other hand, GR level was correlated only with Hsp90 level, and this
   correlation was evident in current PTSD and trauma control groups. In
   conclusion, PTSD and exposure to trauma are not related to changes in
   lymphocyte MR, Hsp90 or Hsp70 levels, but may be associated with
   disturbances in corticosteroid receptors interaction with heat shock
   proteins. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
T2  - Psychiatry Research
T1  - Mineralocorticoid receptor and heat shock protein expression levels in
 peripheral lymphocytes from war trauma-exposed men with and without PTSD
IS  - 2
VL  - 215
DO  - 10.1016/j.psychres.2013.11.022
SP  - 379
EP  - 385
ER  - 

@article{
author = "Matić, Gordana and Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Elaković, Ivana and Manitašević Jovanović, Sanja and Elzaedi, Younis Mouftah and Perisic, Tatjana and Dunderski, Jadranka and Damjanovic, Svetozar and Knezevic, Goran and Spiric, Zeljko and Vermetten, Eric and Savic, Danka",
year = "2014",
abstract = "Alterations in the number and functional status of mineralocorticoid
   (MR) and glucocorticoid receptors (GR) may contribute to vulnerability
   to posttraumatic stress disorder (PTSD). Corticosteroid receptors are
   chaperoned by heat shock proteins Hsp90 and Hsp70. We examined relations
   between corticosteroid receptor and heat shock protein expression
   levels, and related them with war trauma exposure, PTSD and resilience
   to PTSD. Relative levels of MR. Hsp90 and Hsp70 were determined by
   immunoblotting in lymphocytes from war trauma-exposed men with current
   PTSD (current PTSD group, n=113), with lifetime PTSD (life-time PTSD
   group, n=61) and without PTSD (trauma control group, n=88), and from
   non-traumatized healthy controls (healthy control group, n=85).
   Between-group differences in MR, Hsp90 and Hsp70 levels and in MR/GR
   ratio were not observed. The level of MR was correlated with both Hsp90
   and Hsp70 levels in trauma control and healthy control groups. On the
   other hand, GR level was correlated only with Hsp90 level, and this
   correlation was evident in current PTSD and trauma control groups. In
   conclusion, PTSD and exposure to trauma are not related to changes in
   lymphocyte MR, Hsp90 or Hsp70 levels, but may be associated with
   disturbances in corticosteroid receptors interaction with heat shock
   proteins. (C) 2013 Elsevier Ireland Ltd. All rights reserved.",
journal = "Psychiatry Research",
title = "Mineralocorticoid receptor and heat shock protein expression levels in
 peripheral lymphocytes from war trauma-exposed men with and without PTSD",
number = "2",
volume = "215",
doi = "10.1016/j.psychres.2013.11.022",
pages = "379-385"
}

Matić, G., Vojnović-Milutinović, D., Brkljačić, J., Elaković, I., Manitašević Jovanović, S., Elzaedi, Y. M., Perisic, T., Dunderski, J., Damjanovic, S., Knezevic, G., Spiric, Z., Vermetten, E.,& Savic, D.. (2014). Mineralocorticoid receptor and heat shock protein expression levels in
 peripheral lymphocytes from war trauma-exposed men with and without PTSD. in Psychiatry Research, 215(2), 379-385.
https://doi.org/10.1016/j.psychres.2013.11.022

Matić G, Vojnović-Milutinović D, Brkljačić J, Elaković I, Manitašević Jovanović S, Elzaedi YM, Perisic T, Dunderski J, Damjanovic S, Knezevic G, Spiric Z, Vermetten E, Savic D. Mineralocorticoid receptor and heat shock protein expression levels in
 peripheral lymphocytes from war trauma-exposed men with and without PTSD. in Psychiatry Research. 2014;215(2):379-385.
doi:10.1016/j.psychres.2013.11.022 .

Matić, Gordana, Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Elaković, Ivana, Manitašević Jovanović, Sanja, Elzaedi, Younis Mouftah, Perisic, Tatjana, Dunderski, Jadranka, Damjanovic, Svetozar, Knezevic, Goran, Spiric, Zeljko, Vermetten, Eric, Savic, Danka, "Mineralocorticoid receptor and heat shock protein expression levels in
 peripheral lymphocytes from war trauma-exposed men with and without PTSD" in Psychiatry Research, 215, no. 2 (2014):379-385,
https://doi.org/10.1016/j.psychres.2013.11.022 . .

TY  - JOUR
AU  - Brkljačić, Jelena
AU  - Glban, Alhadi M.
AU  - Mijuskovic, Ana
AU  - Nikolić-Kokić, Aleksandra
AU  - Elaković, Ivana
AU  - Velickovic, Natasa
AU  - Matić, Gordana
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2192
AB  - Increased fructose consumption is correlated with the rising prevalence
   of obesity, metabolic syndrome, and type 2 diabetes. It is believed that
   reactive oxygen species contribute to the development and progression of
   metabolic disturbances, especially those associated with insulin
   resistance. Dietary fructose produces both pro-oxidative and
   antioxidative effects, depending upon the experimental conditions,
   dosage, duration of treatment, and pathophysiological milieu. The
   effects of fructose overconsumption on young populations, which have an
   increased risk of developing metabolic disorders in adulthood, have not
   been fully elucidated. We have previously shown that rats subjected to a
   long-term fructose-enriched diet immediately after weaning display
   impaired hepatic insulin sensitivity. In this study, we tested the
   hypothesis that long-term fructose consumption induces alterations in
   the redox setting of the liver. Starting from the 21st day afterbirth,
   male Wistar rats were maintained for 9 weeks on a standard diet
   (control) or a fructose-enriched diet that consisted of standard food
   and 10\% fructose solution instead of drinking water. The expression and
   activity of antioxidant enzymes as well as lipid peroxidation and
   protein damage markers were measured. The results showed that a
   fructose-enriched diet led to an increased expression of mitochondrial
   manganese superoxide dismutase but did not affect antioxidant enzymes
   activity, lipid peroxidation, thiol content, and the level of protein
   oxidation. Therefore, our results suggest that the decrease in hepatic
   insulin sensitivity that was previously observed in rats that were kept
   on the same diet regime might be attributed to molecular mechanisms
   other than redox disbalance. A possible fructose-related micronutrient
   deficiency should be examined. (C) 2014 Elsevier Inc. All rights
   reserved.
T2  - Nutrition Research
T1  - Long-term fructose-enriched diet introduced immediately after weaning
 does not induce oxidative stress in the rat liver
IS  - 7
VL  - 34
DO  - 10.1016/j.nutres.2014.06.006
SP  - 646
EP  - 652
ER  - 

@article{
author = "Brkljačić, Jelena and Glban, Alhadi M. and Mijuskovic, Ana and Nikolić-Kokić, Aleksandra and Elaković, Ivana and Velickovic, Natasa and Matić, Gordana",
year = "2014",
abstract = "Increased fructose consumption is correlated with the rising prevalence
   of obesity, metabolic syndrome, and type 2 diabetes. It is believed that
   reactive oxygen species contribute to the development and progression of
   metabolic disturbances, especially those associated with insulin
   resistance. Dietary fructose produces both pro-oxidative and
   antioxidative effects, depending upon the experimental conditions,
   dosage, duration of treatment, and pathophysiological milieu. The
   effects of fructose overconsumption on young populations, which have an
   increased risk of developing metabolic disorders in adulthood, have not
   been fully elucidated. We have previously shown that rats subjected to a
   long-term fructose-enriched diet immediately after weaning display
   impaired hepatic insulin sensitivity. In this study, we tested the
   hypothesis that long-term fructose consumption induces alterations in
   the redox setting of the liver. Starting from the 21st day afterbirth,
   male Wistar rats were maintained for 9 weeks on a standard diet
   (control) or a fructose-enriched diet that consisted of standard food
   and 10\% fructose solution instead of drinking water. The expression and
   activity of antioxidant enzymes as well as lipid peroxidation and
   protein damage markers were measured. The results showed that a
   fructose-enriched diet led to an increased expression of mitochondrial
   manganese superoxide dismutase but did not affect antioxidant enzymes
   activity, lipid peroxidation, thiol content, and the level of protein
   oxidation. Therefore, our results suggest that the decrease in hepatic
   insulin sensitivity that was previously observed in rats that were kept
   on the same diet regime might be attributed to molecular mechanisms
   other than redox disbalance. A possible fructose-related micronutrient
   deficiency should be examined. (C) 2014 Elsevier Inc. All rights
   reserved.",
journal = "Nutrition Research",
title = "Long-term fructose-enriched diet introduced immediately after weaning
 does not induce oxidative stress in the rat liver",
number = "7",
volume = "34",
doi = "10.1016/j.nutres.2014.06.006",
pages = "646-652"
}

Brkljačić, J., Glban, A. M., Mijuskovic, A., Nikolić-Kokić, A., Elaković, I., Velickovic, N.,& Matić, G.. (2014). Long-term fructose-enriched diet introduced immediately after weaning
 does not induce oxidative stress in the rat liver. in Nutrition Research, 34(7), 646-652.
https://doi.org/10.1016/j.nutres.2014.06.006

Brkljačić J, Glban AM, Mijuskovic A, Nikolić-Kokić A, Elaković I, Velickovic N, Matić G. Long-term fructose-enriched diet introduced immediately after weaning
 does not induce oxidative stress in the rat liver. in Nutrition Research. 2014;34(7):646-652.
doi:10.1016/j.nutres.2014.06.006 .

Brkljačić, Jelena, Glban, Alhadi M., Mijuskovic, Ana, Nikolić-Kokić, Aleksandra, Elaković, Ivana, Velickovic, Natasa, Matić, Gordana, "Long-term fructose-enriched diet introduced immediately after weaning
 does not induce oxidative stress in the rat liver" in Nutrition Research, 34, no. 7 (2014):646-652,
https://doi.org/10.1016/j.nutres.2014.06.006 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Lukić, Iva
AU  - Mitić, Milos Z
AU  - Đorđević, Jelena D
AU  - Elaković, Ivana
AU  - Đorđević, Ana
AU  - Krstić-Demonacos, Marija
AU  - Matić, Gordana
AU  - Radojcić, Marija B
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/940
AB  - Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.
T2  - Psychoneuroendocrinology
T1  - Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism
IS  - 12
VL  - 38
SP  - 1459
EP  - 2924
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_940
ER  - 

@article{
author = "Adžić, Miroslav and Lukić, Iva and Mitić, Milos Z and Đorđević, Jelena D and Elaković, Ivana and Đorđević, Ana and Krstić-Demonacos, Marija and Matić, Gordana and Radojcić, Marija B",
year = "2013",
abstract = "Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.",
journal = "Psychoneuroendocrinology",
title = "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism",
number = "12",
volume = "38",
pages = "1459-2924",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_940"
}

Adžić, M., Lukić, I., Mitić, M. Z., Đorđević, J. D., Elaković, I., Đorđević, A., Krstić-Demonacos, M., Matić, G.,& Radojcić, M. B.. (2013). Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology, 38(12), 1459-2924.
https://hdl.handle.net/21.15107/rcub_ibiss_940

Adžić M, Lukić I, Mitić MZ, Đorđević JD, Elaković I, Đorđević A, Krstić-Demonacos M, Matić G, Radojcić MB. Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology. 2013;38(12):1459-2924.
https://hdl.handle.net/21.15107/rcub_ibiss_940 .

Adžić, Miroslav, Lukić, Iva, Mitić, Milos Z, Đorđević, Jelena D, Elaković, Ivana, Đorđević, Ana, Krstić-Demonacos, Marija, Matić, Gordana, Radojcić, Marija B, "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism" in Psychoneuroendocrinology, 38, no. 12 (2013):1459-2924,
https://hdl.handle.net/21.15107/rcub_ibiss_940 .

TY  - JOUR
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
AU  - Elaković, Ivana
AU  - Tanić, Nikola
PY  - 2013
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/501
AB  - Real-time RT PCR has been recognized as an accurate, reliable and sensitive method for quantifying gene transcription. However, several steps preceding PCR represent critical points and source of inaccuracies. These steps include cell processing, RNA extraction, RNA storage, assessment of RNA concentration and cDNA synthesis. To compensate for potential variability introduced by the procedure, normalization of target gene expression has been established. Accurate normalization has become an absolute prerequisite for the correct quantification of gene expression. Several strategies are in use for the normalization of data, including normalization to sample size, to total RNA or to an internal reference. Among these, the use of housekeeping genes as an internal (endogenous) control is the most common approach. Given the increased sensitivity, reproducibility and large dynamic range of this methodology, the requirements for a proper reference gene for normalization have become increasingly stringent. The aim of this paper is to discuss the concept of normalization in mRNA quantification, as well as to discuss several statistical algorithms developed to help the validation of potential reference genes. By showing that the use of inappropriate endogenous control might lead to incorrect results and misinterpretation of experimental data, we are joining the creators of Minimum Information for Publication of Quantitative Real-Time PCR Experiments (MIQE) in an attempt to convince scientists that proper validation of potential reference genes is an absolute prerequisite for correct normalization and, therefore, for providing accurate and reliable data by quantitative real-time RT PCR gene expression analyses.
AB  - RT-PCR je prepoznat kao precizna, pouzdana i osetljiva metoda za kvantifikaciju transkripcije gena. Međutim, ovoj metodi prethodi nekoliko koraka koji predstavljaju kritične tačke i izvor potencijalnih grešaka. Ovi koraci uključuju obradu ćelijskog materijala, ekstrakciju i čuvanje RNK, određivanje koncentracije RNK i sintezu cDNK. Da bi se kompenzovala potencijalna varijabilnost nastala tokom procedure, uvedena je normalizacija ekspresije ciljnih gena. Precizna normalizacija je postala apsolutni preduslov za tačnu kvantifikaciju ekspresije gena. Postoji nekoliko strategija za normalizaciju eksperimentalnih podataka, uključujući normalizaciju u odnosu na veličinu uzorka, ukupnu RNK ili internu kontrolu (referencu). Kao interna (endogena) kontrola najčešće se koriste geni sa stabilnom ekspresijom. Imajući u vidu veliku osetljivost, reproducibilnost i veliki dinamički opseg PCR metode, zahtevi za odgovarajućim referentnim genima koji će se koristiti za normalizaciju podataka postali su veoma restriktivni. Cilj ovog rada je da razjasni koncept normalizacije i prokomentariše nekoliko statističkih algoritama koji su razvijeni kako bi pomogli u validaciji potencijalnih referentnih gena. Pokazujući da korišćenje neodgovarajućih referentnih gena (endogenih kontrola) može da dovede do netačnih rezultata i pogrešne interpretacije eksperimentalnih podataka, mi se priključujemo tvorcima uputstva MIQE (eng. Minimum Information for Publication of Quantitative Real-Time PCR Experiments) u pokušaju da ubedimo naučnu javnost da je ispravna validacija potencijalnih referentnih gena apsolutni preduslov za tačnu normalizaciju i, shodno tome, preduslov za dobijanje tačnih i pouzdanih podataka u analizi ekspresije gena metodom kvantitativnog PCR-a u realnom vremenu.
T2  - Journal of Medical Biochemistry
T1  - Izučavanje ekspresije gena - kako dobiti tačne i pouzdane podatke kvantitativnim RT PCR-om u realnom vremenu
T1  - Gene expression studies: How to obtain accurate and reliable data by quantitative real-time RT PCR
IS  - 4
VL  - 32
SP  - 325
EP  - 338
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_501
ER  - 

@article{
author = "Matić, Gordana and Brkljačić, Jelena and Elaković, Ivana and Tanić, Nikola",
year = "2013, 2013",
abstract = "Real-time RT PCR has been recognized as an accurate, reliable and sensitive method for quantifying gene transcription. However, several steps preceding PCR represent critical points and source of inaccuracies. These steps include cell processing, RNA extraction, RNA storage, assessment of RNA concentration and cDNA synthesis. To compensate for potential variability introduced by the procedure, normalization of target gene expression has been established. Accurate normalization has become an absolute prerequisite for the correct quantification of gene expression. Several strategies are in use for the normalization of data, including normalization to sample size, to total RNA or to an internal reference. Among these, the use of housekeeping genes as an internal (endogenous) control is the most common approach. Given the increased sensitivity, reproducibility and large dynamic range of this methodology, the requirements for a proper reference gene for normalization have become increasingly stringent. The aim of this paper is to discuss the concept of normalization in mRNA quantification, as well as to discuss several statistical algorithms developed to help the validation of potential reference genes. By showing that the use of inappropriate endogenous control might lead to incorrect results and misinterpretation of experimental data, we are joining the creators of Minimum Information for Publication of Quantitative Real-Time PCR Experiments (MIQE) in an attempt to convince scientists that proper validation of potential reference genes is an absolute prerequisite for correct normalization and, therefore, for providing accurate and reliable data by quantitative real-time RT PCR gene expression analyses., RT-PCR je prepoznat kao precizna, pouzdana i osetljiva metoda za kvantifikaciju transkripcije gena. Međutim, ovoj metodi prethodi nekoliko koraka koji predstavljaju kritične tačke i izvor potencijalnih grešaka. Ovi koraci uključuju obradu ćelijskog materijala, ekstrakciju i čuvanje RNK, određivanje koncentracije RNK i sintezu cDNK. Da bi se kompenzovala potencijalna varijabilnost nastala tokom procedure, uvedena je normalizacija ekspresije ciljnih gena. Precizna normalizacija je postala apsolutni preduslov za tačnu kvantifikaciju ekspresije gena. Postoji nekoliko strategija za normalizaciju eksperimentalnih podataka, uključujući normalizaciju u odnosu na veličinu uzorka, ukupnu RNK ili internu kontrolu (referencu). Kao interna (endogena) kontrola najčešće se koriste geni sa stabilnom ekspresijom. Imajući u vidu veliku osetljivost, reproducibilnost i veliki dinamički opseg PCR metode, zahtevi za odgovarajućim referentnim genima koji će se koristiti za normalizaciju podataka postali su veoma restriktivni. Cilj ovog rada je da razjasni koncept normalizacije i prokomentariše nekoliko statističkih algoritama koji su razvijeni kako bi pomogli u validaciji potencijalnih referentnih gena. Pokazujući da korišćenje neodgovarajućih referentnih gena (endogenih kontrola) može da dovede do netačnih rezultata i pogrešne interpretacije eksperimentalnih podataka, mi se priključujemo tvorcima uputstva MIQE (eng. Minimum Information for Publication of Quantitative Real-Time PCR Experiments) u pokušaju da ubedimo naučnu javnost da je ispravna validacija potencijalnih referentnih gena apsolutni preduslov za tačnu normalizaciju i, shodno tome, preduslov za dobijanje tačnih i pouzdanih podataka u analizi ekspresije gena metodom kvantitativnog PCR-a u realnom vremenu.",
journal = "Journal of Medical Biochemistry",
title = "Izučavanje ekspresije gena - kako dobiti tačne i pouzdane podatke kvantitativnim RT PCR-om u realnom vremenu, Gene expression studies: How to obtain accurate and reliable data by quantitative real-time RT PCR",
number = "4",
volume = "32",
pages = "325-338",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_501"
}

Matić, G., Brkljačić, J., Elaković, I.,& Tanić, N.. (2013). Izučavanje ekspresije gena - kako dobiti tačne i pouzdane podatke kvantitativnim RT PCR-om u realnom vremenu. in Journal of Medical Biochemistry, 32(4), 325-338.
https://hdl.handle.net/21.15107/rcub_ibiss_501

Matić G, Brkljačić J, Elaković I, Tanić N. Izučavanje ekspresije gena - kako dobiti tačne i pouzdane podatke kvantitativnim RT PCR-om u realnom vremenu. in Journal of Medical Biochemistry. 2013;32(4):325-338.
https://hdl.handle.net/21.15107/rcub_ibiss_501 .

Matić, Gordana, Brkljačić, Jelena, Elaković, Ivana, Tanić, Nikola, "Izučavanje ekspresije gena - kako dobiti tačne i pouzdane podatke kvantitativnim RT PCR-om u realnom vremenu" in Journal of Medical Biochemistry, 32, no. 4 (2013):325-338,
https://hdl.handle.net/21.15107/rcub_ibiss_501 .

TY  - JOUR
AU  - Matić, Gordana
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Elaković, Ivana
AU  - Manitašević-Jovanović, Sanja
AU  - Perišić, Tatjana
AU  - Dunđerski, Jadranka S.
AU  - Damjanović, Svetozar S
AU  - Knežević, Goran
AU  - Spirić, Zeljko M
AU  - Vermetten, Eric
AU  - Savić, Danka A
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/999
AB  - Objective: Posttraumatic stress disorder (PTSD) has been shown to be associated with altered glucocorticoid receptor (GR) activity. We studied the expression and functional properties of the receptor in peripheral blood mononuclear cells (PBMCs) from non-traumatized healthy individuals (healthy controls; n = 85), and war trauma-exposed individuals with current PTSD (n = 113), with life-time PTSD (n = 61) and without PTSD (trauma controls; n = 88). The aim of the study was to distinguish the receptor alterations related to PTSD from those related to trauma itself or to resilience to PTSD. Methods: Functional status of the receptor was assessed by radioligand binding and lysozyme synthesis inhibition assays. The level of GR gene expression was measured by quantitative PCR and immunoblotting. Results: Current PTSD patients had the lowest, while trauma controls had the highest number of glucocorticoid binding sites (B-max) in PBMCs. Hormone-binding potential (B-max/K-D ratio) of the receptor was diminished in the current PTSD group in comparison to all other study groups. Correlation between B-max and K-D that normally exists in healthy individuals was decreased in the current PTSD group. Contrasting B-max data, GR protein level was lower in trauma controls than in participants with current or life-time PTSD. Conclusions: Current PTSD is characterized by reduced lymphocyte GR hormone-binding potential and by disturbed compensation between B-max and hormone-binding affinity. Resilience to PTSD is associated with enlarged fraction of the receptor molecules capable of hormone binding, within the total receptor molecule population in PBMCs. (C) 2013 Elsevier Inc. All rights reserved.
T2  - Progress in Neuro-Psychopharmacology & Biological Psychiatry
T1  - Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD
IS  - null
VL  - 43
SP  - 63
EP  - 245
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_999
ER  - 

@article{
author = "Matić, Gordana and Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Elaković, Ivana and Manitašević-Jovanović, Sanja and Perišić, Tatjana and Dunđerski, Jadranka S. and Damjanović, Svetozar S and Knežević, Goran and Spirić, Zeljko M and Vermetten, Eric and Savić, Danka A",
year = "2013",
abstract = "Objective: Posttraumatic stress disorder (PTSD) has been shown to be associated with altered glucocorticoid receptor (GR) activity. We studied the expression and functional properties of the receptor in peripheral blood mononuclear cells (PBMCs) from non-traumatized healthy individuals (healthy controls; n = 85), and war trauma-exposed individuals with current PTSD (n = 113), with life-time PTSD (n = 61) and without PTSD (trauma controls; n = 88). The aim of the study was to distinguish the receptor alterations related to PTSD from those related to trauma itself or to resilience to PTSD. Methods: Functional status of the receptor was assessed by radioligand binding and lysozyme synthesis inhibition assays. The level of GR gene expression was measured by quantitative PCR and immunoblotting. Results: Current PTSD patients had the lowest, while trauma controls had the highest number of glucocorticoid binding sites (B-max) in PBMCs. Hormone-binding potential (B-max/K-D ratio) of the receptor was diminished in the current PTSD group in comparison to all other study groups. Correlation between B-max and K-D that normally exists in healthy individuals was decreased in the current PTSD group. Contrasting B-max data, GR protein level was lower in trauma controls than in participants with current or life-time PTSD. Conclusions: Current PTSD is characterized by reduced lymphocyte GR hormone-binding potential and by disturbed compensation between B-max and hormone-binding affinity. Resilience to PTSD is associated with enlarged fraction of the receptor molecules capable of hormone binding, within the total receptor molecule population in PBMCs. (C) 2013 Elsevier Inc. All rights reserved.",
journal = "Progress in Neuro-Psychopharmacology & Biological Psychiatry",
title = "Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD",
number = "null",
volume = "43",
pages = "63-245",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_999"
}

Matić, G., Vojnović-Milutinović, D., Brkljačić, J., Elaković, I., Manitašević-Jovanović, S., Perišić, T., Dunđerski, J. S., Damjanović, S. S., Knežević, G., Spirić, Z. M., Vermetten, E.,& Savić, D. A.. (2013). Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD. in Progress in Neuro-Psychopharmacology & Biological Psychiatry, 43(null), 63-245.
https://hdl.handle.net/21.15107/rcub_ibiss_999

Matić G, Vojnović-Milutinović D, Brkljačić J, Elaković I, Manitašević-Jovanović S, Perišić T, Dunđerski JS, Damjanović SS, Knežević G, Spirić ZM, Vermetten E, Savić DA. Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD. in Progress in Neuro-Psychopharmacology & Biological Psychiatry. 2013;43(null):63-245.
https://hdl.handle.net/21.15107/rcub_ibiss_999 .

Matić, Gordana, Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Elaković, Ivana, Manitašević-Jovanović, Sanja, Perišić, Tatjana, Dunđerski, Jadranka S., Damjanović, Svetozar S, Knežević, Goran, Spirić, Zeljko M, Vermetten, Eric, Savić, Danka A, "Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD" in Progress in Neuro-Psychopharmacology & Biological Psychiatry, 43, no. null (2013):63-245,
https://hdl.handle.net/21.15107/rcub_ibiss_999 .

TY  - JOUR
AU  - Đorđević, Ana
AU  - Đorđević, Jelena D
AU  - Elaković, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radojcić, Marija B
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1211
AB  - Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Progress in Neuro-Psychopharmacology & Biological Psychiatry
T1  - Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats
IS  - 1
VL  - 36
EP  - 100
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1211
ER  - 

@article{
author = "Đorđević, Ana and Đorđević, Jelena D and Elaković, Ivana and Adžić, Miroslav and Matić, Gordana and Radojcić, Marija B",
year = "2012",
abstract = "Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Progress in Neuro-Psychopharmacology & Biological Psychiatry",
title = "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats",
number = "1",
volume = "36",
pages = "100",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1211"
}

Đorđević, A., Đorđević, J. D., Elaković, I., Adžić, M., Matić, G.,& Radojcić, M. B.. (2012). Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. in Progress in Neuro-Psychopharmacology & Biological Psychiatry, 36(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1211

Đorđević A, Đorđević JD, Elaković I, Adžić M, Matić G, Radojcić MB. Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. in Progress in Neuro-Psychopharmacology & Biological Psychiatry. 2012;36(1):null-100.
https://hdl.handle.net/21.15107/rcub_ibiss_1211 .

Đorđević, Ana, Đorđević, Jelena D, Elaković, Ivana, Adžić, Miroslav, Matić, Gordana, Radojcić, Marija B, "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats" in Progress in Neuro-Psychopharmacology & Biological Psychiatry, 36, no. 1 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1211 .

TY  - JOUR
AU  - Đorđević, Ana
AU  - Đorđević, Jelena D
AU  - Elaković, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radojcić, Marija B
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1094
AB  - The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex
IS  - 1-3
VL  - 693
SP  - 375
EP  - 44
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1094
ER  - 

@article{
author = "Đorđević, Ana and Đorđević, Jelena D and Elaković, Ivana and Adžić, Miroslav and Matić, Gordana and Radojcić, Marija B",
year = "2012",
abstract = "The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex",
number = "1-3",
volume = "693",
pages = "375-44",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1094"
}

Đorđević, A., Đorđević, J. D., Elaković, I., Adžić, M., Matić, G.,& Radojcić, M. B.. (2012). Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology, 693(1-3), 375-44.
https://hdl.handle.net/21.15107/rcub_ibiss_1094

Đorđević A, Đorđević JD, Elaković I, Adžić M, Matić G, Radojcić MB. Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology. 2012;693(1-3):375-44.
https://hdl.handle.net/21.15107/rcub_ibiss_1094 .

Đorđević, Ana, Đorđević, Jelena D, Elaković, Ivana, Adžić, Miroslav, Matić, Gordana, Radojcić, Marija B, "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex" in European Journal of Pharmacology, 693, no. 1-3 (2012):375-44,
https://hdl.handle.net/21.15107/rcub_ibiss_1094 .

TY  - JOUR
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Tanić, Nikola
AU  - Bursać, Biljana
AU  - Teofilović, Ana
AU  - Veličković, Nataša
AU  - Elaković, Ivana
AU  - Matić, Gordana
PY  - 2012
UR  - https://www.ingentaconnect.com/content/asp/asl/2012/00000005/00000002/art00019%3bjsessionid=4lrjbbnfmh61v.x-ic-live-03
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3463
AB  - Selection of appropriate endogenous control for normalization in a specific experimental paradigm is a critical step in the quantification of gene expression. The aim of this study was to identify suitable reference gene(s) for simultaneous normalization of gene expression in liver and adipose tissue of control and fructose-fed male rats which is considered as model of metabolic syndrome. Using TaqMan Real Time RT-PCR, we carried out an extensive evaluation of five frequently used endogenous controls, b-actin, b2-microglobulin, 18S rRNA, hypoxanthine phosphoribosyl transferase 1 and TATA box binding protein, for their presumed stability of expression.
Expression stability was analyzed by GeNorm and NormFinder software packages, and by direct comparison of Ct values. Both, GeNorm and NormFinder identified  2-microglobulin in the liver, hypoxanthine phosphoribosyl transferase 1 in the adipose tissue and TATA box binding protein for comparative analysis of the two tissues as
most stable genes. The combination of b-actin and TATA box binding protein in the liver, hypoxanthine phosphoribosyl transferase 1 and TATA box binding protein in the adipose tissue and b-actin and TATA box binding protein for both tissues together appeared to be the most suitable combinations of reference genes for studying
alterations in gene expression in fructose-fed rats.
T2  - Advanced Science Letters
T1  - Identification of Suitable Reference Genes for Gene Expression Studies in Tissues from Fructose-Fed Rats
IS  - 2
VL  - 5
DO  - 10.1166/asl.2012.2186
SP  - 560
EP  - 565(6)
ER  - 

@article{
author = "Đorđević, Ana and Vojnović-Milutinović, Danijela and Tanić, Nikola and Bursać, Biljana and Teofilović, Ana and Veličković, Nataša and Elaković, Ivana and Matić, Gordana",
year = "2012",
abstract = "Selection of appropriate endogenous control for normalization in a specific experimental paradigm is a critical step in the quantification of gene expression. The aim of this study was to identify suitable reference gene(s) for simultaneous normalization of gene expression in liver and adipose tissue of control and fructose-fed male rats which is considered as model of metabolic syndrome. Using TaqMan Real Time RT-PCR, we carried out an extensive evaluation of five frequently used endogenous controls, b-actin, b2-microglobulin, 18S rRNA, hypoxanthine phosphoribosyl transferase 1 and TATA box binding protein, for their presumed stability of expression.
Expression stability was analyzed by GeNorm and NormFinder software packages, and by direct comparison of Ct values. Both, GeNorm and NormFinder identified  2-microglobulin in the liver, hypoxanthine phosphoribosyl transferase 1 in the adipose tissue and TATA box binding protein for comparative analysis of the two tissues as
most stable genes. The combination of b-actin and TATA box binding protein in the liver, hypoxanthine phosphoribosyl transferase 1 and TATA box binding protein in the adipose tissue and b-actin and TATA box binding protein for both tissues together appeared to be the most suitable combinations of reference genes for studying
alterations in gene expression in fructose-fed rats.",
journal = "Advanced Science Letters",
title = "Identification of Suitable Reference Genes for Gene Expression Studies in Tissues from Fructose-Fed Rats",
number = "2",
volume = "5",
doi = "10.1166/asl.2012.2186",
pages = "560-565(6)"
}

Đorđević, A., Vojnović-Milutinović, D., Tanić, N., Bursać, B., Teofilović, A., Veličković, N., Elaković, I.,& Matić, G.. (2012). Identification of Suitable Reference Genes for Gene Expression Studies in Tissues from Fructose-Fed Rats. in Advanced Science Letters, 5(2), 560-565(6).
https://doi.org/10.1166/asl.2012.2186

Đorđević A, Vojnović-Milutinović D, Tanić N, Bursać B, Teofilović A, Veličković N, Elaković I, Matić G. Identification of Suitable Reference Genes for Gene Expression Studies in Tissues from Fructose-Fed Rats. in Advanced Science Letters. 2012;5(2):560-565(6).
doi:10.1166/asl.2012.2186 .

Đorđević, Ana, Vojnović-Milutinović, Danijela, Tanić, Nikola, Bursać, Biljana, Teofilović, Ana, Veličković, Nataša, Elaković, Ivana, Matić, Gordana, "Identification of Suitable Reference Genes for Gene Expression Studies in Tissues from Fructose-Fed Rats" in Advanced Science Letters, 5, no. 2 (2012):560-565(6),
https://doi.org/10.1166/asl.2012.2186 . .