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  - 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 . .