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  - JOUR
AU  - Glban, Alhadi M.
AU  - Teofilović, Ana
AU  - Velickovic, Natasa
AU  - Nikolić-Kokić, Aleksandra
AU  - Blagojević, Duško
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1914
AB  - BACKGROUNDIncreased fructose consumption correlates with rising
   prevalence of various metabolic disorders, some of which were linked to
   oxidative stress. The relationship between fructose consumption and
   oxidative stress is complex and effects of a fructose-rich diet on the
   young population have not been fully elucidated. The aim of this study
   was to investigate whether high-fructose diet applied in the period from
   weaning to adulthood induces oxidative stress in the liver, thus
   contributing to induction or aggravation of metabolic disturbances in
   later adulthood. To that end we examined the effects of high-fructose
   diet on expression and activity of antioxidant enzymes, markers of lipid
   peroxidation and protein damage in the liver as the main fructose
   metabolizing tissue.
   RESULTSHigh-fructose diet increased only SOD2 (mitochondrial manganese
   superoxide dismutase) activity, with no effect on other antioxidant
   enzymes, lipid peroxidation or accumulation of damaged proteins in the
   liver.
   CONCLUSIONThe results show that fructose-induced metabolic disturbances
   could not be attributed to oxidative stress, at least not at young age.
   The absence of oxidative stress in the liver observed herein implies
   that young organisms are capable of maintaining redox homeostasis when
   challenged by fructose-derived energy overload. (c) 2014 Society of
   Chemical Industry
T2  - Journal of the Science of Food and Agriculture
T1  - The expression and activity of antioxidant enzymes in the liver of rats
 exposed to high-fructose diet in the period from weaning to adulthood
IS  - 11
VL  - 95
DO  - 10.1002/jsfa.6953
SP  - 2319
EP  - 2324
ER  - 

@article{
author = "Glban, Alhadi M. and Teofilović, Ana and Velickovic, Natasa and Nikolić-Kokić, Aleksandra and Blagojević, Duško and Matić, Gordana and Brkljačić, Jelena",
year = "2015",
abstract = "BACKGROUNDIncreased fructose consumption correlates with rising
   prevalence of various metabolic disorders, some of which were linked to
   oxidative stress. The relationship between fructose consumption and
   oxidative stress is complex and effects of a fructose-rich diet on the
   young population have not been fully elucidated. The aim of this study
   was to investigate whether high-fructose diet applied in the period from
   weaning to adulthood induces oxidative stress in the liver, thus
   contributing to induction or aggravation of metabolic disturbances in
   later adulthood. To that end we examined the effects of high-fructose
   diet on expression and activity of antioxidant enzymes, markers of lipid
   peroxidation and protein damage in the liver as the main fructose
   metabolizing tissue.
   RESULTSHigh-fructose diet increased only SOD2 (mitochondrial manganese
   superoxide dismutase) activity, with no effect on other antioxidant
   enzymes, lipid peroxidation or accumulation of damaged proteins in the
   liver.
   CONCLUSIONThe results show that fructose-induced metabolic disturbances
   could not be attributed to oxidative stress, at least not at young age.
   The absence of oxidative stress in the liver observed herein implies
   that young organisms are capable of maintaining redox homeostasis when
   challenged by fructose-derived energy overload. (c) 2014 Society of
   Chemical Industry",
journal = "Journal of the Science of Food and Agriculture",
title = "The expression and activity of antioxidant enzymes in the liver of rats
 exposed to high-fructose diet in the period from weaning to adulthood",
number = "11",
volume = "95",
doi = "10.1002/jsfa.6953",
pages = "2319-2324"
}

Glban, A. M., Teofilović, A., Velickovic, N., Nikolić-Kokić, A., Blagojević, D., Matić, G.,& Brkljačić, J.. (2015). The expression and activity of antioxidant enzymes in the liver of rats
 exposed to high-fructose diet in the period from weaning to adulthood. in Journal of the Science of Food and Agriculture, 95(11), 2319-2324.
https://doi.org/10.1002/jsfa.6953

Glban AM, Teofilović A, Velickovic N, Nikolić-Kokić A, Blagojević D, Matić G, Brkljačić J. The expression and activity of antioxidant enzymes in the liver of rats
 exposed to high-fructose diet in the period from weaning to adulthood. in Journal of the Science of Food and Agriculture. 2015;95(11):2319-2324.
doi:10.1002/jsfa.6953 .

Glban, Alhadi M., Teofilović, Ana, Velickovic, Natasa, Nikolić-Kokić, Aleksandra, Blagojević, Duško, Matić, Gordana, Brkljačić, Jelena, "The expression and activity of antioxidant enzymes in the liver of rats
 exposed to high-fructose diet in the period from weaning to adulthood" in Journal of the Science of Food and Agriculture, 95, no. 11 (2015):2319-2324,
https://doi.org/10.1002/jsfa.6953 . .

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 . .