TY  - JOUR
AU  - Đorđević, Ana
AU  - Bursac, Biljana
AU  - Velickovic, Natasa
AU  - Teofilović, Ana
AU  - Matić, Gordana
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2015
AB  - Objectives: High fructose diet has been shown to have damaging effects
   on the hippocampus, a brain region critical for learning and memory.
   Fructose-induced hippocampal dysfunction may arise from insulin
   resistance and inflammation, and from concomitant changes in
   plasticity-related presynaptic proteins. We hypothesized that long-term
   access to fructose (10\% and 60\% solutions over a period of 9 weeks)
   affects insulin sensitivity, hippocampal inflammation, and synaptic
   plasticity in male Wistar rats.
   Methods: We used the area under curve (AUC) glucose value and inhibitory
   Ser(307) phosphorylation of hippocampal insulin receptor substrate 1
   (IRS-1) as hallmarks of insulin resistance. To examine inflammatory
   state, we analysed protein levels and intracellular redistribution of
   glucocorticoid receptor and nuclear factor-kappa B (NF kappa B), as well
   as mRNA levels of tumour necrosis factor-alpha (TNF-alpha),
   interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta). Polysialylated
   neural cell adhesion molecule (PSA-NCAM) protein was used as a synaptic
   plasticity marker.
   Results: The results indicate different impacts of diverse
   fructose-enriched diets on insulin sensitivity and hippocampal
   inflammation and plasticity. Long-term ingestion of 10\% fructose
   solution led to increase in AUC glucose value, as well as to elevation
   in hippocampal IRS-1 Ser(307) phosphorylation and increase in IL-6 mRNA.
   In rats consuming 60\% fructose, the level of PSA-NCAM was reduced, in
   parallel with augmented glucocorticoid signalization.
   Discussion: The results showed that long-term consumption of 10\%
   fructose solution induces hippocampal insulin resistance and
   inflammation, with no concomitant plasticity changes. Interestingly,
   rats fed with higher concentrations of fructose displayed impaired
   plastic response of the hippocampus, coinciding with augmented
   glucocorticoid signalling, which may provide a basis for cognitive
   deficits associated with metabolic syndrome.
T2  - Nutritional Neuroscience
T1  - The impact of different fructose loads on insulin sensitivity,
 inflammation, and PSA-NCAM-mediated plasticity in the hippocampus of
 fructose-fed male rats
IS  - 2
VL  - 18
DO  - 10.1179/1476830513Y.0000000098
SP  - 66
EP  - 75
ER  - 

@article{
author = "Đorđević, Ana and Bursac, Biljana and Velickovic, Natasa and Teofilović, Ana and Matić, Gordana",
year = "2015",
abstract = "Objectives: High fructose diet has been shown to have damaging effects
   on the hippocampus, a brain region critical for learning and memory.
   Fructose-induced hippocampal dysfunction may arise from insulin
   resistance and inflammation, and from concomitant changes in
   plasticity-related presynaptic proteins. We hypothesized that long-term
   access to fructose (10\% and 60\% solutions over a period of 9 weeks)
   affects insulin sensitivity, hippocampal inflammation, and synaptic
   plasticity in male Wistar rats.
   Methods: We used the area under curve (AUC) glucose value and inhibitory
   Ser(307) phosphorylation of hippocampal insulin receptor substrate 1
   (IRS-1) as hallmarks of insulin resistance. To examine inflammatory
   state, we analysed protein levels and intracellular redistribution of
   glucocorticoid receptor and nuclear factor-kappa B (NF kappa B), as well
   as mRNA levels of tumour necrosis factor-alpha (TNF-alpha),
   interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta). Polysialylated
   neural cell adhesion molecule (PSA-NCAM) protein was used as a synaptic
   plasticity marker.
   Results: The results indicate different impacts of diverse
   fructose-enriched diets on insulin sensitivity and hippocampal
   inflammation and plasticity. Long-term ingestion of 10\% fructose
   solution led to increase in AUC glucose value, as well as to elevation
   in hippocampal IRS-1 Ser(307) phosphorylation and increase in IL-6 mRNA.
   In rats consuming 60\% fructose, the level of PSA-NCAM was reduced, in
   parallel with augmented glucocorticoid signalization.
   Discussion: The results showed that long-term consumption of 10\%
   fructose solution induces hippocampal insulin resistance and
   inflammation, with no concomitant plasticity changes. Interestingly,
   rats fed with higher concentrations of fructose displayed impaired
   plastic response of the hippocampus, coinciding with augmented
   glucocorticoid signalling, which may provide a basis for cognitive
   deficits associated with metabolic syndrome.",
journal = "Nutritional Neuroscience",
title = "The impact of different fructose loads on insulin sensitivity,
 inflammation, and PSA-NCAM-mediated plasticity in the hippocampus of
 fructose-fed male rats",
number = "2",
volume = "18",
doi = "10.1179/1476830513Y.0000000098",
pages = "66-75"
}

Đorđević, A., Bursac, B., Velickovic, N., Teofilović, A.,& Matić, G.. (2015). The impact of different fructose loads on insulin sensitivity,
 inflammation, and PSA-NCAM-mediated plasticity in the hippocampus of
 fructose-fed male rats. in Nutritional Neuroscience, 18(2), 66-75.
https://doi.org/10.1179/1476830513Y.0000000098

Đorđević A, Bursac B, Velickovic N, Teofilović A, Matić G. The impact of different fructose loads on insulin sensitivity,
 inflammation, and PSA-NCAM-mediated plasticity in the hippocampus of
 fructose-fed male rats. in Nutritional Neuroscience. 2015;18(2):66-75.
doi:10.1179/1476830513Y.0000000098 .

Đorđević, Ana, Bursac, Biljana, Velickovic, Natasa, Teofilović, Ana, Matić, Gordana, "The impact of different fructose loads on insulin sensitivity,
 inflammation, and PSA-NCAM-mediated plasticity in the hippocampus of
 fructose-fed male rats" in Nutritional Neuroscience, 18, no. 2 (2015):66-75,
https://doi.org/10.1179/1476830513Y.0000000098 . .

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  - Drakulic, Dunja
AU  - Stanojlovic, Milos
AU  - Nedeljkovic, Nadezda
AU  - Grkovic, Ivana
AU  - Velickovic, Natasa
AU  - Gusevac, Ivana
AU  - Mitrovic, Natasa
AU  - Buzadzic, Ivana
AU  - Horvat, Anica
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1982
AB  - Although dexamethasone (DEX), a synthetic glucocorticoid receptor (GR)
   analog with profound effects on energy metabolism, immune system, and
   hypothalamic-pituitary-adrenal axis, is widely used therapeutically, its
   impact on the brain is poorly understood. The aim of the present study
   was to explore the effect of repeated low-dose DEX administration on the
   activity and expression of the ectonucleotidase enzymes which hydrolyze
   and therefore control extracellular ATP and adenosine concentrations in
   the synaptic cleft. Ectonucleotidases tested were ectonucleoside
   triphosphate diphosphohydrolase 1-3 (NTPDase1-3) and
   ecto-5'-nucleotidase (eN), whereas the effects were evaluated in two
   brain areas that show different sensitivity to glucocorticoid action,
   hippocampus, and cerebral cortex. In the hippocampus, but not in
   cerebral cortex, modest level of neurodegenerative changes as well as
   increase in ATP, ADP, and AMP hydrolysis and upregulation of NTPDase1
   and eN mRNA expression ensued under the influence of DEX. The observed
   pattern of ectonucleotidase activation, which creates tissue volume with
   enhanced capacity for adenosine formation, is the hallmark of the
   response after different insults to the brain.
T2  - Journal of Molecular Neuroscience
T1  - Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and
 Ecto-5'-Nucleotidase in Rat Hippocampus after Repeated Low-Dose
 Dexamethasone Administration
IS  - 4
VL  - 55
DO  - 10.1007/s12031-014-0452-y
SP  - 959
EP  - 967
ER  - 

@article{
author = "Drakulic, Dunja and Stanojlovic, Milos and Nedeljkovic, Nadezda and Grkovic, Ivana and Velickovic, Natasa and Gusevac, Ivana and Mitrovic, Natasa and Buzadzic, Ivana and Horvat, Anica",
year = "2015",
abstract = "Although dexamethasone (DEX), a synthetic glucocorticoid receptor (GR)
   analog with profound effects on energy metabolism, immune system, and
   hypothalamic-pituitary-adrenal axis, is widely used therapeutically, its
   impact on the brain is poorly understood. The aim of the present study
   was to explore the effect of repeated low-dose DEX administration on the
   activity and expression of the ectonucleotidase enzymes which hydrolyze
   and therefore control extracellular ATP and adenosine concentrations in
   the synaptic cleft. Ectonucleotidases tested were ectonucleoside
   triphosphate diphosphohydrolase 1-3 (NTPDase1-3) and
   ecto-5'-nucleotidase (eN), whereas the effects were evaluated in two
   brain areas that show different sensitivity to glucocorticoid action,
   hippocampus, and cerebral cortex. In the hippocampus, but not in
   cerebral cortex, modest level of neurodegenerative changes as well as
   increase in ATP, ADP, and AMP hydrolysis and upregulation of NTPDase1
   and eN mRNA expression ensued under the influence of DEX. The observed
   pattern of ectonucleotidase activation, which creates tissue volume with
   enhanced capacity for adenosine formation, is the hallmark of the
   response after different insults to the brain.",
journal = "Journal of Molecular Neuroscience",
title = "Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and
 Ecto-5'-Nucleotidase in Rat Hippocampus after Repeated Low-Dose
 Dexamethasone Administration",
number = "4",
volume = "55",
doi = "10.1007/s12031-014-0452-y",
pages = "959-967"
}

Drakulic, D., Stanojlovic, M., Nedeljkovic, N., Grkovic, I., Velickovic, N., Gusevac, I., Mitrovic, N., Buzadzic, I.,& Horvat, A.. (2015). Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and
 Ecto-5'-Nucleotidase in Rat Hippocampus after Repeated Low-Dose
 Dexamethasone Administration. in Journal of Molecular Neuroscience, 55(4), 959-967.
https://doi.org/10.1007/s12031-014-0452-y

Drakulic D, Stanojlovic M, Nedeljkovic N, Grkovic I, Velickovic N, Gusevac I, Mitrovic N, Buzadzic I, Horvat A. Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and
 Ecto-5'-Nucleotidase in Rat Hippocampus after Repeated Low-Dose
 Dexamethasone Administration. in Journal of Molecular Neuroscience. 2015;55(4):959-967.
doi:10.1007/s12031-014-0452-y .

Drakulic, Dunja, Stanojlovic, Milos, Nedeljkovic, Nadezda, Grkovic, Ivana, Velickovic, Natasa, Gusevac, Ivana, Mitrovic, Natasa, Buzadzic, Ivana, Horvat, Anica, "Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and
 Ecto-5'-Nucleotidase in Rat Hippocampus after Repeated Low-Dose
 Dexamethasone Administration" in Journal of Molecular Neuroscience, 55, no. 4 (2015):959-967,
https://doi.org/10.1007/s12031-014-0452-y . .

TY  - JOUR
AU  - Petrovic, Snjezana
AU  - Milosevic, Maja
AU  - Ristic-Medic, Danijela
AU  - Velickovic, Natasa
AU  - Drakulic, Dunja
AU  - Grkovic, Ivana
AU  - Horvat, Anica
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2077
AB  - Our earlier studies found that in vitro estradiol modulates
   mitochondrial Ca2+ transport in discrete brain regions. The present
   study examined the role of estradiol receptors (ERs) in
   estradiol-induced inhibition of Ca2+ efflux from synaptosomal
   mitochondria isolated from rat caudate nuclei and brain stems.
   Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for
   Ca2+ transport monitoring. The results revealed that in the presence of
   ER antagonist 7 alpha, 17 beta-{[}9{[}(4,4,5,5,5-pentafluoropentyl)
   sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu
   mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux
   was more than 60\% decreased, suggesting the involvement of ER in this
   mode of estradiol neuromodulatory action. When particular contributions
   of ER alpha and ER beta were tested, it was found that ER beta agonist
   2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+
   efflux more than 20\%, while the inhibition with ER alpha agonist 4,4',
   4''-(4-propyl-{[}1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was
   about 10\%, both compared to the control. Both agonists demonstrated
   attenuation of Ca2+ efflux decrease in the presence of mitochondrial
   Na+/Ca2+ exchanger antagonist
   7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one
   (10 mu mol/L), showing interference with the inhibitory action of that
   agent. Our results strongly indicate ERs as the mediators of
   estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate
   nucleus and brain stem synaptosomes.
T2  - Turkish Journal of Biology
T1  - Estradiol receptors mediate estradiol-induced inhibition of
 mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem
IS  - 2
VL  - 39
DO  - 10.3906/biy-1408-62
SP  - 328
EP  - 334
ER  - 

@article{
author = "Petrovic, Snjezana and Milosevic, Maja and Ristic-Medic, Danijela and Velickovic, Natasa and Drakulic, Dunja and Grkovic, Ivana and Horvat, Anica",
year = "2015",
abstract = "Our earlier studies found that in vitro estradiol modulates
   mitochondrial Ca2+ transport in discrete brain regions. The present
   study examined the role of estradiol receptors (ERs) in
   estradiol-induced inhibition of Ca2+ efflux from synaptosomal
   mitochondria isolated from rat caudate nuclei and brain stems.
   Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for
   Ca2+ transport monitoring. The results revealed that in the presence of
   ER antagonist 7 alpha, 17 beta-{[}9{[}(4,4,5,5,5-pentafluoropentyl)
   sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu
   mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux
   was more than 60\% decreased, suggesting the involvement of ER in this
   mode of estradiol neuromodulatory action. When particular contributions
   of ER alpha and ER beta were tested, it was found that ER beta agonist
   2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+
   efflux more than 20\%, while the inhibition with ER alpha agonist 4,4',
   4''-(4-propyl-{[}1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was
   about 10\%, both compared to the control. Both agonists demonstrated
   attenuation of Ca2+ efflux decrease in the presence of mitochondrial
   Na+/Ca2+ exchanger antagonist
   7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one
   (10 mu mol/L), showing interference with the inhibitory action of that
   agent. Our results strongly indicate ERs as the mediators of
   estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate
   nucleus and brain stem synaptosomes.",
journal = "Turkish Journal of Biology",
title = "Estradiol receptors mediate estradiol-induced inhibition of
 mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem",
number = "2",
volume = "39",
doi = "10.3906/biy-1408-62",
pages = "328-334"
}

Petrovic, S., Milosevic, M., Ristic-Medic, D., Velickovic, N., Drakulic, D., Grkovic, I.,& Horvat, A.. (2015). Estradiol receptors mediate estradiol-induced inhibition of
 mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem. in Turkish Journal of Biology, 39(2), 328-334.
https://doi.org/10.3906/biy-1408-62

Petrovic S, Milosevic M, Ristic-Medic D, Velickovic N, Drakulic D, Grkovic I, Horvat A. Estradiol receptors mediate estradiol-induced inhibition of
 mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem. in Turkish Journal of Biology. 2015;39(2):328-334.
doi:10.3906/biy-1408-62 .

Petrovic, Snjezana, Milosevic, Maja, Ristic-Medic, Danijela, Velickovic, Natasa, Drakulic, Dunja, Grkovic, Ivana, Horvat, Anica, "Estradiol receptors mediate estradiol-induced inhibition of
 mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem" in Turkish Journal of Biology, 39, no. 2 (2015):328-334,
https://doi.org/10.3906/biy-1408-62 . .

TY  - JOUR
AU  - Teofilović, Ana
AU  - Bursac, Biljana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Radovanović, Marina
AU  - Matić, Gordana
AU  - Velickovic, Natasa
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2166
AB  - High fructose consumption provokes metabolic perturbations that result
   in chronic low-grade inflammation and insulin resistance.
   Glucocorticoids, potent anti-inflammatory hormones, have important role
   in pathogenesis of diet-induced metabolic disturbances. The aim of this
   study was to examine the link between glucocorticoid metabolism and
   inflammation in the liver of fructose-fed rats.
   Fructose-fed male Wistar rats consumed 60 \% fructose solution for 9
   weeks. Glucocorticoid prereceptor metabolism and signaling were analyzed
   by measuring the level of 11 beta-hydroxysteroid dehydrogenase type 1
   (11 beta HSD1) and hexose-6-phosphate dehydrogenase expression, as well
   as via determination of intracellular corticosterone concentration,
   glucocorticoid receptor subcellular distribution and expression of its
   target gene, phosphoenolpyruvate carboxykinase. Nuclear factor kappa B
   (NF kappa B), tumor necrosis factor alpha (TNF alpha) and the level of
   inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1) on
   Ser(307) were analyzed as markers of hepatic inflammation. The protein
   and/or mRNA levels of all examined molecules were assessed by Western
   blot and/or qPCR.
   Fructose-rich diet led to an enhancement of 11 beta HSD1 protein level
   in the liver, without affecting intracellular level of corticosterone
   and downstream glucocorticoid signaling. On the other hand,
   proinflammatory state was achieved through NF kappa B activation and
   increased TNF alpha expression, while elevated level of inhibitory
   phosphorylation of IRS-1 was observed as an early hallmark of insulin
   resistance.
   High-fructose diet does not influence hepatic glucocorticoid signaling
   downstream of the receptor, permitting development of NF kappa B-driven
   inflammation. The alteration in 11 beta HSD1 expression is most likely
   the consequence of enhanced inflammation, finally leading to disruption
   of insulin signaling in the rat liver.
T2  - European Journal of Nutrition
T1  - Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats
IS  - 6
VL  - 53
DO  - 10.1007/s00394-013-0641-4
SP  - 1393
EP  - 1402
ER  - 

@article{
author = "Teofilović, Ana and Bursac, Biljana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Radovanović, Marina and Matić, Gordana and Velickovic, Natasa",
year = "2014",
abstract = "High fructose consumption provokes metabolic perturbations that result
   in chronic low-grade inflammation and insulin resistance.
   Glucocorticoids, potent anti-inflammatory hormones, have important role
   in pathogenesis of diet-induced metabolic disturbances. The aim of this
   study was to examine the link between glucocorticoid metabolism and
   inflammation in the liver of fructose-fed rats.
   Fructose-fed male Wistar rats consumed 60 \% fructose solution for 9
   weeks. Glucocorticoid prereceptor metabolism and signaling were analyzed
   by measuring the level of 11 beta-hydroxysteroid dehydrogenase type 1
   (11 beta HSD1) and hexose-6-phosphate dehydrogenase expression, as well
   as via determination of intracellular corticosterone concentration,
   glucocorticoid receptor subcellular distribution and expression of its
   target gene, phosphoenolpyruvate carboxykinase. Nuclear factor kappa B
   (NF kappa B), tumor necrosis factor alpha (TNF alpha) and the level of
   inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1) on
   Ser(307) were analyzed as markers of hepatic inflammation. The protein
   and/or mRNA levels of all examined molecules were assessed by Western
   blot and/or qPCR.
   Fructose-rich diet led to an enhancement of 11 beta HSD1 protein level
   in the liver, without affecting intracellular level of corticosterone
   and downstream glucocorticoid signaling. On the other hand,
   proinflammatory state was achieved through NF kappa B activation and
   increased TNF alpha expression, while elevated level of inhibitory
   phosphorylation of IRS-1 was observed as an early hallmark of insulin
   resistance.
   High-fructose diet does not influence hepatic glucocorticoid signaling
   downstream of the receptor, permitting development of NF kappa B-driven
   inflammation. The alteration in 11 beta HSD1 expression is most likely
   the consequence of enhanced inflammation, finally leading to disruption
   of insulin signaling in the rat liver.",
journal = "European Journal of Nutrition",
title = "Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats",
number = "6",
volume = "53",
doi = "10.1007/s00394-013-0641-4",
pages = "1393-1402"
}

Teofilović, A., Bursac, B., Đorđević, A., Vojnović-Milutinović, D., Radovanović, M., Matić, G.,& Velickovic, N.. (2014). Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats. in European Journal of Nutrition, 53(6), 1393-1402.
https://doi.org/10.1007/s00394-013-0641-4

Teofilović A, Bursac B, Đorđević A, Vojnović-Milutinović D, Radovanović M, Matić G, Velickovic N. Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats. in European Journal of Nutrition. 2014;53(6):1393-1402.
doi:10.1007/s00394-013-0641-4 .

Teofilović, Ana, Bursac, Biljana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Radovanović, Marina, Matić, Gordana, Velickovic, Natasa, "Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats" in European Journal of Nutrition, 53, no. 6 (2014):1393-1402,
https://doi.org/10.1007/s00394-013-0641-4 . .

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  - 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 . .