IL-17 Regulates Adipogenesis, Glucose Homeostasis, and Obesity JOURNAL OF IMMUNOLOGY Zuniga, L. A., Shen, W., Joyce-Shaikh, B., Pyatnova, E. A., Richards, A. G., Thom, C., Andrade, S. M., Cua, D. J., Kraemer, F. B., Butcher, E. C. 2010; 185 (11): 6947-6959

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 ?d 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.

View details for DOI 10.4049/jimmunol.1001269

View details for Web of Science ID 000284311500062

View details for PubMedID 21037091

View details for PubMedCentralID PMC3001125