Increased expression of FGF1-mediated signaling molecules in adipose tissue of obese mice
J. physiol. biochem
; 72(2): 157-167, jun. 2016. tab, ilus, graf
Article
em En
| IBECS
| ID: ibc-168263
Biblioteca responsável:
ES1.1
Localização: BNCS
ABSTRACT
Fibroblast growth factors (FGFs) are pleiotropic growth factors that control cell proliferation, migration, and differentiation. Herein, we evaluated whether visceral adiposity of mice is accompanied by the alteration of signaling molecules mediated by fibroblast growth factor receptor 1 (FGFR1) induced by using two different male C57BL/6J mice models of obesity namely high-fat diet (HFD)-induced obesity for 12 weeks or mice with genetic deletion of leptin (ob/ob). Both HFD-fed and ob/ob mice exhibited significantly higher messenger RNA (mRNA) levels of FGF1, cyclin D (cycD), transcription factor E2F1, peroxisome proliferator-activated receptor-gamma 2 (PPAR-γ2), CCAAT-enhancer-binding protein alpha (C/EBPα), and adipocyte protein 2 (aP2) genes in their epididymal adipose tissues compared to those of the normal diet (ND)-fed and lean control mice, respectively. In addition, immunoblot analyses of the epididymal adipose tissues revealed that both mice exposed to HFD and ob/ob mice exhibited elevated phosphorylation of FGFR1, extracellular-signal-regulated kinase (ERK), and retinoblastoma (Rb) proteins. These data support the notion that FGF1-mediated signaling represents an important signaling cascade related to adipogenesis, at least partially, among other known signaling pathways. These new findings regarding the molecular mechanisms controlling adipose tissue plasticity provide a novel insight about the functional network with potential therapeutic application against obesity (AU)
RESUMEN
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Coleções:
06-national
/
ES
Base de dados:
IBECS
Assunto principal:
Transdução de Sinais
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Regulação para Cima
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Fator 1 de Crescimento de Fibroblastos
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Receptor Tipo 1 de Fator de Crescimento de Fibroblastos
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Adiposidade
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Tecido Adiposo Branco
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Obesidade
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
J. physiol. biochem
Ano de publicação:
2016
Tipo de documento:
Article