Department of Immunobiology and Pharmacological Genetics, Graduate School of Medicine and Pharmaceutical Science for Research, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan.
Nutrients. 2013 Sep 23;5(9):3757-78. doi: 10.3390/nu5093757.
Obesity-associated chronic tissue inflammation is a key contributing factor to type 2 diabetes mellitus, and a number of studies have clearly demonstrated that the immune system and metabolism are highly integrated. Recent advances in deciphering the various immune cells and signaling networks that link the immune and metabolic systems have contributed to our understanding of the pathogenesis of obesity-associated inflammation. Other recent studies have suggested that pattern recognition receptors in the innate immune system recognize various kinds of endogenous and exogenous ligands, and have a crucial role in initiating or promoting obesity-associated chronic inflammation. Importantly, these mediators act on insulin target cells or on insulin-producing cells impairing insulin sensitivity and its secretion. Here, we discuss how various pattern recognition receptors in the immune system underlie the etiology of obesity-associated inflammation and insulin resistance, with a particular focus on the TLR (Toll-like receptor) family protein Radioprotective 105 (RP105)/myeloid differentiation protein-1 (MD-1).
肥胖相关的慢性组织炎症是 2 型糖尿病的一个重要致病因素，许多研究已经明确表明免疫系统和代谢是高度整合的。近年来，人们在破译将免疫系统和代谢系统联系起来的各种免疫细胞和信号网络方面取得了进展，这有助于我们理解肥胖相关炎症的发病机制。其他最近的研究表明，先天免疫系统中的模式识别受体识别各种内源性和外源性配体，并在启动或促进肥胖相关慢性炎症中起着关键作用。重要的是，这些介质作用于胰岛素靶细胞或胰岛素产生细胞，损害胰岛素敏感性及其分泌。在这里，我们讨论了免疫系统中的各种模式识别受体如何构成肥胖相关炎症和胰岛素抵抗的病因学基础，特别关注 Toll 样受体 (TLR) 家族蛋白 Radioprotective 105 (RP105)/髓样分化蛋白-1 (MD-1)。
