| First Author | Zúñiga LA | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 11 | Pages | 6947-59 |
| PubMed ID | 21037091 | Mgi Jnum | J:166142 |
| Mgi Id | MGI:4839832 | Doi | 10.4049/jimmunol.1001269 |
| Citation | Zuniga LA, et al. (2010) IL-17 Regulates Adipogenesis, Glucose Homeostasis, and Obesity. J Immunol 185(11):6947-59 |
| abstractText | 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 gammadelta 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. |
