胰岛素抵抗
脂肪组织
促炎细胞因子
炎症
白色脂肪组织
内科学
内分泌学
基因敲除
脂肪组织巨噬细胞
胰岛素
生物
医学
生物化学
细胞凋亡
作者
Ning Wang,Hor‐Yue Tan,Sha Li,Di Wang,Yu Xu,Cheng Zhang,Xiaozhong Wen,Chi‐Ming Che,Yibin Feng
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2019-08-02
卷期号:5 (8)
被引量:18
标识
DOI:10.1126/sciadv.aav0198
摘要
Proinflammatory activation and accumulation of adipose tissue macrophages (ATMs) are associated with increased risk of insulin resistance in obesity. Here, we described the previously unidentified role of selenocysteine insertion sequence-binding protein 2 (SBP2) in maintaining insulin sensitivity in obesity. SBP2 was suppressed in ATMs of diet-induced obese mice and was correlated with adipose tissue inflammation. Loss of SBP2 initiated metabolic activation of ATMs, inducing intracellular reactive oxygen species content and inflammasome, which subsequently promoted IL-1β-associated local proliferation and infiltration of proinflammatory macrophages. ATM-specific knockdown of SBP2 in obese mice promoted insulin resistance by increasing fat tissue inflammation and expansion. Reexpression of SBP2 improved insulin sensitivity. Last, an herbal formula that specifically induced SBP2 expression in ATMs can experimentally improve insulin sensitivity. Clinical observation revealed that it improved hyperglycemia in patients with diabetes. This study identified SBP2 in ATMs as a potential target in rescuing insulin resistance in obesity.
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