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Type: Artigo de periódico
Title: Jnk And Ikkβ Phosphorylation Is Reduced By Glucocorticoids In Adipose Tissue From Insulin-resistant Rats.
Author: Motta, Katia
Barbosa, Amanda Marreiro
Bobinski, Franciane
Boschero, Antonio Carlos
Rafacho, Alex
Abstract: Peripheral insulin resistance (IR) is one of the main side effects caused by glucocorticoid (GC)-based therapies, and the molecular mechanisms of GC-induced IR are not yet fully elucidated. Thus, we aimed to investigate the effects of dexamethasone treatment on the main components of insulin and inflammatory signaling in the adipose tissue of rats. Male Wistar rats received daily injections of dexamethasone (1mg/kg body weight (b.w.), intraperitoneally (i.p.)) for 5 days (DEX), whereas control rats received saline (CTL). The metabolic status was investigated, and the epididymal fat fragments were collected for lipolysis and western blot analyses. The DEX rats became hyperglycemic, hyperinsulinemic, insulin resistant and glucose intolerant, compared with the CTL rats (P<0.05). The basal glycerol release in the fat fragments was 1.5-fold higher in the DEX rats (P<0.05). The phosphorylation of protein kinase B (PKB) at ser(473) decreased by 44%, whereas, the phosphorylation of insulin receptor substrate (IRS)-1 at ser(307) increased by 93% in the adipose tissue of the DEX rats after an oral bolus of glucose (P<0.05). The basal phosphorylation of c-jun-N-terminal kinase (JNK) and inhibitor of nuclear factor kappa-B (IKKβ) proteins was reduced by 46% and 58%, respectively, in the adipose tissue of the DEX rats (P<0.05). This was paralleled with a significant reduction (47%) in the glucocorticoid receptor (GR) protein content in the adipose tissue of the DEX rats (P<0.05). The insulin-resistant status of rats induced by dexamethasone administration have PKB and IRS-1 activity attenuated in epididymal fat without increases in the phosphorylation of the proinflammatory signals JNK and IKKβ.
Subject: Adipose Tissue
Body Weight
I-kappa B Kinase
Insulin Receptor Substrate Proteins
Insulin Resistance
Map Kinase Kinase 4
Proto-oncogene Proteins C-akt
Pyruvic Acid
Rats, Wistar
Signal Transduction
Toll-like Receptor 4
Glucocorticoid Receptor
Inflammatory Signaling
Insulin Resistance
Insulin Signaling
Citation: The Journal Of Steroid Biochemistry And Molecular Biology. v. 145, p. 1-12, 2015-Jan.
Rights: fechado
Identifier DOI: 10.1016/j.jsbmb.2014.09.024
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

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