Suppr超能文献

炎症小体使肥胖处于危险地带。

The inflammasome puts obesity in the danger zone.

机构信息

Department of Medicine, Radboud University Nijmegen Medical Centre, Nijmegen 6525 GA, The Netherlands.

出版信息

Cell Metab. 2012 Jan 4;15(1):10-8. doi: 10.1016/j.cmet.2011.10.011.

Abstract

Obesity-induced inflammation is an important contributor to the induction of insulin resistance. Recently, the cytokine interleukin-1β (IL-1β) has emerged as a prominent instigator of the proinflammatory response in obesity. Several studies over the last year have subsequently deciphered the molecular mechanisms responsible for IL-1β activation in adipose tissue, liver, and macrophages and demonstrated a central role of the processing enzyme caspase-1 and of the protein complex leading to its activation called the inflammasome. These data suggest that activation of the inflammasome represents a crucial step in the road from obesity to insulin resistance and type 2 diabetes.

摘要

肥胖引起的炎症是导致胰岛素抵抗的一个重要因素。最近,细胞因子白细胞介素-1β(IL-1β)已成为肥胖中促炎反应的主要启动子。过去一年的几项研究随后阐明了负责脂肪组织、肝脏和巨噬细胞中 IL-1β 激活的分子机制,并证明了加工酶半胱天冬酶-1 和导致其激活的蛋白质复合物(称为炎症小体)的核心作用。这些数据表明,炎症小体的激活代表了从肥胖到胰岛素抵抗和 2 型糖尿病的关键步骤。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验