-
- Luis A. Zúñiga
- *Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine;
-
- Wen-Jun Shen
- ‡Division of Endocrinology, Department of Medicine, Stanford University, Stanford, CA 94305;
-
- Barbara Joyce-Shaikh
- §MERCK, Palo Alto, CA 94304
-
- Ekaterina A. Pyatnova
- *Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine;
-
- Andrew G. Richards
- *Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine;
-
- Colin Thom
- *Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine;
-
- Sofia M. Andrade
- *Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine;
-
- Daniel J. Cua
- §MERCK, Palo Alto, CA 94304
-
- Fredric B. Kraemer
- ‡Division of Endocrinology, Department of Medicine, Stanford University, Stanford, CA 94305;
-
- Eugene C. Butcher
- *Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine;
抄録
<jats:title>Abstract</jats:title> <jats:p>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.</jats:p>
収録刊行物
-
- The Journal of Immunology
-
The Journal of Immunology 185 (11), 6947-6959, 2010-12-01
The American Association of Immunologists