期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 118, 期 9, 页码 2992-3002出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI34260
关键词
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资金
- NIH [DK 033651, DK 074868, 5 T32DK007494-24]
- Eunice Kennedy Shriver National Institute of Child Health And Human Development (NICHD)/NIH [U54 HD 012303]
- University of California Discovery Program [bio03-10383]
- American Diabetes Association
Insulin resistance is a major metabolic feature of obesity and is a key factor in the etiology of a number of diseases, including type 2 diabetes. In this review, we discuss potential mechanisms by which brief nutrient excess and obesity lead to insulin resistance and propose that these mechanisms of action are different but interrelated. We discuss how pathways that sense nutrients within skeletal muscle are readily able to regulate insulin action. We then discuss how obesity leads to insulin resistance via a complex interplay among systemic fatty acid excess, microhypoxia in adipose tissue, ER stress, and inflammation. In particular, we focus on the hypothesis that the macrophage is an important cell type in the propagation of inflammation and induction of insulin resistance in obesity. Overall, we provide our integrative perspective regarding how nutrients and obesity interact to regulate insulin sensitivity.
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