Ministry of Education, Science and Technological Development of the Republic of Serbia, Grant OI1613024

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Ministry of Education, Science and Technological Development of the Republic of Serbia, Grant OI1613024

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Fructose and stress induce opposite effects on lipid metabolism in the visceral adipose tissue of adult female rats through glucocorticoid action

Kovačević, Sanja; Brkljačić, Jelena; Matić, Gordana; Elaković, Ivana

(Heidelberg: Springer, 2017)

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 . .
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