IL-17 regulates adipogenesis, glucose homeostasis, and obesity.
J Immunol
; 185(11): 6947-59, 2010 Dec 01.
Article
em En
| MEDLINE
| ID: mdl-21037091
ABSTRACT
Inflammatory mediators have the potential to impact a surprising range of diseases, including obesity and its associated metabolic syndrome. In this paper, we show that the proinflammatory cytokine IL-17 inhibits adipogenesis, moderates adipose tissue (AT) accumulation, and regulates glucose metabolism in mice. IL-17 deficiency enhances diet-induced obesity in mice and accelerates AT accumulation even in mice fed a low-fat diet. In addition to potential systemic effects, IL-17 is expressed locally in AT by leukocytes, predominantly by γδ T cells. IL-17 suppresses adipocyte differentiation from mouse-derived 3T3-L1 preadipocytes in vitro, and inhibits expression of genes encoding proadipogenic transcription factors, adipokines, and molecules involved in lipid and glucose metabolism. IL-17 also acts on differentiated adipocytes, impairing glucose uptake, and young IL-17-deficient mice show enhanced glucose tolerance and insulin sensitivity. Our findings implicate IL-17 as a negative regulator of adipogenesis and glucose metabolism in mice, and show that it delays the development of obesity.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Tecido Adiposo
/
Interleucina-17
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Adipogenia
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Glucose
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Homeostase
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Obesidade
Limite:
Animals
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article