Abstract | PURPOSE: METHODS: RESULTS:
Fructose-rich diet led to an enhancement of 11βHSD1 protein level in the liver, without affecting intracellular level of corticosterone and downstream glucocorticoid signaling. On the other hand, proinflammatory state was achieved through NFκB activation and increased TNFα expression, while elevated level of inhibitory phosphorylation of IRS-1 was observed as an early hallmark of insulin resistance. CONCLUSION: High- fructose diet does not influence hepatic glucocorticoid signaling downstream of the receptor, permitting development of NFκB-driven inflammation. The alteration in 11βHSD1 expression is most likely the consequence of enhanced inflammation, finally leading to disruption of insulin signaling in the rat liver.
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Authors | Ana Vasiljević, Biljana Bursać, Ana Djordjevic, Danijela Vojnović Milutinović, Marina Nikolić, Gordana Matić, Nataša Veličković |
Journal | European journal of nutrition
(Eur J Nutr)
Vol. 53
Issue 6
Pg. 1393-402
(Sep 2014)
ISSN: 1436-6215 [Electronic] Germany |
PMID | 24389792
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Blood Glucose
- Fatty Acids, Nonesterified
- Glucocorticoids
- Insulin Receptor Substrate Proteins
- Irs1 protein, rat
- NF-kappa B
- RNA, Messenger
- Receptors, Glucocorticoid
- Triglycerides
- Tumor Necrosis Factor-alpha
- Fructose
- Carbohydrate Dehydrogenases
- galactose-6-phosphate dehydrogenase
- 11-beta-Hydroxysteroid Dehydrogenase Type 1
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Topics |
- 11-beta-Hydroxysteroid Dehydrogenase Type 1
(genetics, metabolism)
- Adipose Tissue
(drug effects)
- Animals
- Blood Glucose
(metabolism)
- Body Weight
(drug effects)
- Carbohydrate Dehydrogenases
(genetics, metabolism)
- Energy Intake
- Fatty Acids, Nonesterified
(blood)
- Fructose
(administration & dosage, adverse effects)
- Glucocorticoids
(metabolism)
- Inflammation
(etiology, pathology)
- Insulin Receptor Substrate Proteins
(genetics, metabolism)
- Insulin Resistance
- Liver
(drug effects, enzymology, physiopathology)
- Male
- NF-kappa B
(metabolism)
- Phosphorylation
- RNA, Messenger
(genetics, metabolism)
- Rats
- Rats, Wistar
- Receptors, Glucocorticoid
(metabolism)
- Triglycerides
(blood)
- Tumor Necrosis Factor-alpha
(genetics, metabolism)
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