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.

肥胖是获得性胰岛素抵抗的主要原因，正是肥胖在美国的流行导致 2 型糖尿病的发病率显着增加。脂肪细胞功能障碍和慢性低度脂肪组织 (AT) 炎症是胰岛素抵抗的主要原因。AT巨噬细胞（ATM）的异常积累和激活以及ATM内TLR4介导的免疫反应的异常激活是与胰岛素抵抗相关的慢性低度AT炎症的关键特征。我们最近表明，GPR120 在巨噬细胞和脂肪细胞中充当 omega-3 脂肪酸的生理受体，可介导有效的抗炎和胰岛素增敏作用。GPR120 在控制炎症方面的重要作用提高了靶向该受体在包括肥胖和 2 型糖尿病在内的许多炎症性疾病中具有治疗潜力的可能性。在这篇综述论文中，我们讨论了 omega-3 脂肪酸感应 GPR120，并强调了靶向该受体在改善疾病方面的潜在结果。