Jnk And Ikk Beta Phosphorylation Is Reduced By Glucocorticoids In Adipose Tissue From Insulin-resistant Rats

dc.creatorMotta
dc.creatorKatia; Barbosa
dc.creatorAmanda Marreiro; Bobinski
dc.creatorFranciane; Boschero
dc.creatorAntonio Carlos; Rafacho
dc.creatorAlex
dc.date2015-JAN
dc.date2016-06-07T13:14:35Z
dc.date2016-06-07T13:14:35Z
dc.date.accessioned2018-03-29T01:35:21Z
dc.date.available2018-03-29T01:35:21Z
dc.identifier
dc.identifierJnk And Ikk Beta Phosphorylation Is Reduced By Glucocorticoids In Adipose Tissue From Insulin-resistant Rats. Pergamon-elsevier Science Ltd, v. 145, p. 1-12 JAN-2015.
dc.identifier0960-0760
dc.identifierWOS:000347771400001
dc.identifier10.1016/j.jsbmb.2014.09.024
dc.identifierhttp://www.sciencedirect.com/science/article/pii/S0960076014002234
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/241668
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1305366
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionObjectives: 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. Materials/methods: Male Wistar rats received daily injections of dexamethasone (1 mg/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. Results: 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 (IKK beta) 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). Conclusion: 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 IKK beta. (C) 2014 Elsevier Ltd. All rights reserved.
dc.description145
dc.description
dc.description
dc.description1
dc.description12
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionCNPq [471397/2011-3]
dc.description
dc.description
dc.description
dc.languageen
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD
dc.publisher
dc.publisherOXFORD
dc.relationJOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
dc.rightsfechado
dc.sourceWOS
dc.subjectDexamethasone-treated Rats
dc.subjectNf-kappa-b
dc.subjectDiet-induced Obesity
dc.subjectProtein-kinase-b
dc.subjectReceptor Substrate-1
dc.subjectPhosphatidylinositol 3-kinase
dc.subjectGlucose-homeostasis
dc.subjectEndocrine Pancreas
dc.subjectC-jun
dc.subjectInflammation
dc.titleJnk And Ikk Beta Phosphorylation Is Reduced By Glucocorticoids In Adipose Tissue From Insulin-resistant Rats
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución