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Type: Artigo de periódico
Title: Quercetin decreases inflammatory response and increases insulin action in skeletal muscle of ob/ob mice and in L6 myotubes
Author: Anhe, Gabriel F.
Okamoto, Maristela M.
Kinote, Andrezza
Sollon, Carolina
Lellis-Santos, Camilo
Anhe, Fernando F.
Lima, Guilherme A.
Hirabara, Sandro M.
Velloso, Licio A.
Bordin, Silvana
Machado, Ubiratan F.
Abstract: Quercetin is a potent anti-inflammatory flavonoid, but its capacity to modulate insulin sensitivity in obese insulin resistant conditions is unknown. This study investigated the effect of quercetin treatment upon insulin sensitivity of ob/ob mice and its potential molecular mechanisms. Obese ob/ob mice were treated with quercetin for 10 weeks, and L6 myotubes were treated with either palmitate or tumor necrosis factor-alpha (TNF alpha) plus quercetin. Cells and muscles were processed for analysis of glucose transporter 4 (GLUT4), TNF alpha and inducible nitric oxide synthase (iNOS) expression, and c-Jun N-terminal kinase (JNK) and inhibitor of nuclear factor-kappa B (NF-kappa B) kinase (I kappa K) phosphorylation. Myotubes were assayed for glucose uptake and NF-kappa B translocation. Chromatin immunoprecipitation assessed NF-kappa B binding to GLUT4 promoter. Quercetin treatment improved whole body insulin sensitivity by increasing GLUT4 expression and decreasing JNK phosphorylation, and TNF alpha and iNOS expression in skeletal muscle. Quercetin suppressed palmitate-induced upregulation of TNF alpha and iNOS and restored normal levels of GLUT4 in myotubes. In parallel, quercetin suppressed TNF alpha-induced reduction of glucose uptake in myotubes. Nuclear accumulation of NF-kappa B in myotubes and binding of NF-kappa B to GLUT4 promoter in muscles of ob/ob mice were also reduced by quercetin. We demonstrated that quercetin decreased the inflammatory status in skeletal muscle of obese mice and in L6 myotubes. This effect was followed by increased muscle GLUT4, with parallel improvement of insulin sensitivity. These results point out quercetin as a putative strategy to manage inflammatory-related insulin resistance. (C) 2012 Elsevier B.V. All rights reserved.
Subject: Flavonoids
Insulin resistance
Editor: Elsevier
Citation: European Journal of Pharmacology. Elsevier, v.689, n.41334, p.285-293, 2012
Rights: fechado
Identifier DOI: 10.1016/j.ejphar.2012.06.007
Date Issue: 2012
Appears in Collections:FCM - Artigos e Outros Documentos

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