胰岛素受体
肥胖
泛素
胰岛素
内科学
内分泌学
细胞生物学
癌症研究
化学
作者
Tomoki Abe,Katsuya Hirasaka,Shohei Kohno,Arisa Ochi,Naoko Yamagishi,Ayako Ohno,Shigetada Teshima-Kondo,Takeshi Nikawa
出处
期刊:Endocrine Journal
[The Japan Endocrine Society]
日期:2014-01-01
卷期号:61 (6): 529-538
被引量:16
标识
DOI:10.1507/endocrj.ej14-0048
摘要
Obesity causes type 2 diabetes, atherosclerosis and cardiovascular diseases by inducing systemic insulin resistance. It is now recognized that obesity is related to chronic low-grade inflammation in adipose tissue. Specifically, activated immune cells infiltrate adipose tissue and cause inflammation. There is increasing evidence that activated macrophages accumulate in the hypertrophied adipose tissue of rodents and humans and induce systemic insulin resistance by secreting inflammatory cytokines. Accordingly, a better understanding of the molecular mechanisms underlying macrophage activation in adipose tissue will facilitate the development of new therapeutic strategies. Currently, little is known about the regulation of macrophage activation, although E3 ubiquitin ligase Casitas B-lineage lymphoma (Cbl)-b was identified recently as a novel negative regulator of macrophage activation in adipose tissue. Cbl-b, which is a suppressor of T- and B-cell activation, inhibits intracellular signal transduction by targeting some tyrosine kinases. Notably, preventing Cbl-b-mediated macrophage activation improves obesity-induced insulin resistance in mice. c-Cbl is another member of the Cbl family that is associated with insulin resistance in obesity. These reports suggest that Cbl-b and c-Cbl are potential therapeutic targets for treating obesity-induced insulin resistance. In this review, we focus on the importance of Cbl-b in macrophage activation in aging-induced and high-fat diet-induced obesity.
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