| Literature DB >> 27050305 |
Byung-Cheol Lee1, Myung-Sunny Kim2, Munkyong Pae3, Yasuhiko Yamamoto3, Delphine Eberlé3, Takeshi Shimada3, Nozomu Kamei3, Hee-Sook Park4, Souphatta Sasorith3, Ju Rang Woo3, Jia You3, William Mosher3, Hugh J M Brady5, Steven E Shoelson3, Jongsoon Lee6.
Abstract
Obesity-induced inflammation mediated by immune cells in adipose tissue appears to participate in the pathogenesis of insulin resistance. We show that natural killer (NK) cells in adipose tissue play an important role. High-fat diet (HFD) increases NK cell numbers and the production of proinflammatory cytokines, notably TNFα, in epididymal, but not subcutaneous, fat depots. When NK cells were depleted either with neutralizing antibodies or genetic ablation in E4bp4(+/-) mice, obesity-induced insulin resistance improved in parallel with decreases in both adipose tissue macrophage (ATM) numbers, and ATM and adipose tissue inflammation. Conversely, expansion of NK cells following IL-15 administration or reconstitution of NK cells into E4bp4(-/-) mice increased both ATM numbers and adipose tissue inflammation and exacerbated HFD-induced insulin resistance. These results indicate that adipose NK cells control ATMs as an upstream regulator potentially by producing proinflammatory mediators, including TNFα, and thereby contribute to the development of obesity-induced insulin resistance.Entities:
Mesh：
Year: 2016 PMID： 27050305 PMCID： PMC4833527 DOI： 10.1016/j.cmet.2016.03.002
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 27.287