omega-3脂肪酸受体GPR120在胰岛素抵抗中的作用。

International journal of obesity supplements Pub Date : 2014-07-01 Epub Date: 2014-07-08 DOI:10.1038/ijosup.2014.5
D Y Oh, E Walenta
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引用次数: 7

摘要

肥胖是获得性胰岛素抵抗的主要原因,肥胖在美国的流行导致了2型糖尿病发病率的显著增加。脂肪细胞功能障碍和慢性低级别脂肪组织(AT)炎症是胰岛素抵抗的主要原因。AT巨噬细胞(ATMs)的异常积聚和激活以及ATMs内tlr4介导的免疫应答的异常激活是胰岛素抵抗相关的慢性低度AT炎症的关键特征。我们最近的研究表明,GPR120在巨噬细胞和脂肪细胞中作为omega-3脂肪酸的生理受体,介导有效的抗炎和胰岛素增敏作用。GPR120在炎症控制中的重要作用提高了靶向该受体可能在许多炎症性疾病(包括肥胖和2型糖尿病)中具有治疗潜力的可能性。在这篇综述文章中,我们讨论了omega-3脂肪酸传感GPR120,并强调了靶向该受体在改善疾病中的潜在结果。
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The role of omega-3 fatty acid receptor GPR120 in insulin resistance.

Obesity is the dominant cause of acquired insulin resistance, and it is the epidemic of obesity in the United States that is driving the markedly increasing incidence of type 2 diabetes. Adipocyte dysfunction and chronic low-grade adipose tissue (AT) inflammation are the major causes of insulin resistance. Abnormal accumulation and activation of AT macrophages (ATMs) and abnormal activation of the TLR4-mediated immune responses within ATMs are the key characters of the chronic low-grade AT inflammation associated with insulin resistance. We have recently shown that GPR120 acts as a physiological receptor of omega-3 fatty acid in macrophages and adipocytes, which mediate potent anti-inflammatory and insulin-sensitizing effects. The important role that GPR120 has in the control of inflammation raises the possibility that targeting this receptor could have therapeutic potential in many inflammatory diseases including obesity and type 2 diabetes. In this review paper, we discuss omega-3 fatty acid-sensing GPR120 and highlight the potential outcomes of targeting this receptor in ameliorating disease.

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