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Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress

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2019
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Authors
Velicković, Nataša
Teofilović, Ana
Ilić, Dragana
Đorđević, Ana
Vojnović-Milutinović, Danijela
Petrović, Snježana B.
Preitner, Frederic
Tappy, Luc
Matić, Gordana
Article (Published version)
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Abstract
Purpose High-fructose consumption and chronic stress are both associated with metabolic inflammation and insulin resistance. Recently, disturbed activity of energy sensor AMP-activated protein kinase (AMPK) was recognized as mediator between nutrient-induced stress and inflammation. Thus, we analyzed the effects of high-fructose diet, alone or in combination with chronic stress, on glucose homeostasis, inflammation and expression of energy sensing proteins in the rat liver. Methods In male Wistar rats exposed to 9-week 20% fructose diet and/or 4-week chronic unpredictable stress we measured plasma and hepatic corticosterone level, indicators of glucose homeostasis and lipid metabolism, hepatic inflammation (pro- and anti-inflammatory cytokine levels, Toll-like receptor 4, NLRP3, activation of NF kappa B, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha). Results High-fructose di...et led to glucose intolerance, activation of NF kappa B and JNK pathways and increased intrahepatic IL-1 beta, TNF alpha and inhibitory phosphorylation of insulin receptor substrate 1 on Ser(307). It also decreased phospho-AMPK/AMPK ratio and increased SIRT1 expression. Stress alone increased plasma and hepatic corticosterone but did not influence glucose tolerance, nor hepatic inflammatory or energy-sensing proteins. After the combined treatment, hepatic corticosterone was increased, glucose tolerance remained preserved, while hepatic inflammation was partially prevented despite decreased AMPK activity. Conclusion High-fructose diet resulted in glucose intolerance, hepatic inflammation, decreased AMPK activity and reduced insulin sensitivity. Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids.

Keywords:
Inflammation / AMP-activated protein kinase / Dietary fructose / Stress / Rat liver
Source:
European Journal of Nutrition, 2019, 58, 5, 1829-1845
Publisher:
  • Springer Heidelberg, Heidelberg
Funding / projects:
  • Role of steroid hormones in neuroendocrine adaptation to stress and pathophysiology of metabolic syndrome - molecular mechanisms and clinical implications (RS-41009)
  • SCOPES JRP [IZ73ZO_152331]

DOI: 10.1007/s00394-018-1730-1

ISSN: 1436-6207

PubMed: 29845385

WoS: 000476492800007

Scopus: 2-s2.0-85047661903
[ Google Scholar ]
11
11
URI
http://rimi.imi.bg.ac.rs/handle/123456789/913
Collections
  • Radovi istraživača / Researchers' publications
Institution/Community
Institut za medicinska istraživanja
TY  - JOUR
AU  - Velicković, Nataša
AU  - Teofilović, Ana
AU  - Ilić, Dragana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Petrović, Snježana B.
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2019
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/913
AB  - Purpose High-fructose consumption and chronic stress are both associated with metabolic inflammation and insulin resistance. Recently, disturbed activity of energy sensor AMP-activated protein kinase (AMPK) was recognized as mediator between nutrient-induced stress and inflammation. Thus, we analyzed the effects of high-fructose diet, alone or in combination with chronic stress, on glucose homeostasis, inflammation and expression of energy sensing proteins in the rat liver. Methods In male Wistar rats exposed to 9-week 20% fructose diet and/or 4-week chronic unpredictable stress we measured plasma and hepatic corticosterone level, indicators of glucose homeostasis and lipid metabolism, hepatic inflammation (pro- and anti-inflammatory cytokine levels, Toll-like receptor 4, NLRP3, activation of NF kappa B, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha). Results High-fructose diet led to glucose intolerance, activation of NF kappa B and JNK pathways and increased intrahepatic IL-1 beta, TNF alpha and inhibitory phosphorylation of insulin receptor substrate 1 on Ser(307). It also decreased phospho-AMPK/AMPK ratio and increased SIRT1 expression. Stress alone increased plasma and hepatic corticosterone but did not influence glucose tolerance, nor hepatic inflammatory or energy-sensing proteins. After the combined treatment, hepatic corticosterone was increased, glucose tolerance remained preserved, while hepatic inflammation was partially prevented despite decreased AMPK activity. Conclusion High-fructose diet resulted in glucose intolerance, hepatic inflammation, decreased AMPK activity and reduced insulin sensitivity. Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids.
PB  - Springer Heidelberg, Heidelberg
T2  - European Journal of Nutrition
T1  - Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress
EP  - 1845
IS  - 5
SP  - 1829
VL  - 58
DO  - 10.1007/s00394-018-1730-1
UR  - conv_4592
ER  - 
@article{
author = "Velicković, Nataša and Teofilović, Ana and Ilić, Dragana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Petrović, Snježana B. and Preitner, Frederic and Tappy, Luc and Matić, Gordana",
year = "2019",
abstract = "Purpose High-fructose consumption and chronic stress are both associated with metabolic inflammation and insulin resistance. Recently, disturbed activity of energy sensor AMP-activated protein kinase (AMPK) was recognized as mediator between nutrient-induced stress and inflammation. Thus, we analyzed the effects of high-fructose diet, alone or in combination with chronic stress, on glucose homeostasis, inflammation and expression of energy sensing proteins in the rat liver. Methods In male Wistar rats exposed to 9-week 20% fructose diet and/or 4-week chronic unpredictable stress we measured plasma and hepatic corticosterone level, indicators of glucose homeostasis and lipid metabolism, hepatic inflammation (pro- and anti-inflammatory cytokine levels, Toll-like receptor 4, NLRP3, activation of NF kappa B, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha). Results High-fructose diet led to glucose intolerance, activation of NF kappa B and JNK pathways and increased intrahepatic IL-1 beta, TNF alpha and inhibitory phosphorylation of insulin receptor substrate 1 on Ser(307). It also decreased phospho-AMPK/AMPK ratio and increased SIRT1 expression. Stress alone increased plasma and hepatic corticosterone but did not influence glucose tolerance, nor hepatic inflammatory or energy-sensing proteins. After the combined treatment, hepatic corticosterone was increased, glucose tolerance remained preserved, while hepatic inflammation was partially prevented despite decreased AMPK activity. Conclusion High-fructose diet resulted in glucose intolerance, hepatic inflammation, decreased AMPK activity and reduced insulin sensitivity. Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids.",
publisher = "Springer Heidelberg, Heidelberg",
journal = "European Journal of Nutrition",
title = "Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress",
pages = "1845-1829",
number = "5",
volume = "58",
doi = "10.1007/s00394-018-1730-1",
url = "conv_4592"
}
Velicković, N., Teofilović, A., Ilić, D., Đorđević, A., Vojnović-Milutinović, D., Petrović, S. B., Preitner, F., Tappy, L.,& Matić, G.. (2019). Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress. in European Journal of Nutrition
Springer Heidelberg, Heidelberg., 58(5), 1829-1845.
https://doi.org/10.1007/s00394-018-1730-1
conv_4592
Velicković N, Teofilović A, Ilić D, Đorđević A, Vojnović-Milutinović D, Petrović SB, Preitner F, Tappy L, Matić G. Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress. in European Journal of Nutrition. 2019;58(5):1829-1845.
doi:10.1007/s00394-018-1730-1
conv_4592 .
Velicković, Nataša, Teofilović, Ana, Ilić, Dragana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Petrović, Snježana B., Preitner, Frederic, Tappy, Luc, Matić, Gordana, "Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress" in European Journal of Nutrition, 58, no. 5 (2019):1829-1845,
https://doi.org/10.1007/s00394-018-1730-1 .,
conv_4592 .

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