Shvarts V
Patol Fiziol Eksp Ter. 2010 Jul-Sep(3):45-51.
The data of TLR-4 and TLR-2 existance in adipose tissue cells is presented in the review, their signal pathway is described, and an idea of physiological and pathological role of innate immune system receptors is given proof. TLRs activation leads to insulin resistance of adipose, hepatic and muscle cells, which increases glucose and lipids level in blood. This reaction is defined as a condition of physiological insulin resistance, which role is in providing immune processes with energetic and plastic substances. Ligands of TLRs are components of microorganisms: bacterial lipoproteins and liopolysacharides, as well as nonsaturated fatty acids. Inadequate uptake of the latter with food activates TLR-4 and R-2, acting as a mechanism for pathological alterations. Under the conditions of innate imunity receptors excessive activation, there is an adipose tissue inflammation, overproduction of cytokines, along with insulin resistance. It promotes the progress of obesity, diabetes and atherosclerosis.
综述中呈现了脂肪组织细胞中TLR - 4和TLR - 2存在的数据,描述了它们的信号通路,并给出了先天免疫系统受体生理和病理作用的证据。TLRs激活会导致脂肪、肝脏和肌肉细胞的胰岛素抵抗,从而使血液中的葡萄糖和脂质水平升高。这种反应被定义为生理性胰岛素抵抗状态,其作用是为免疫过程提供能量和可塑性物质。TLRs的配体是微生物的成分:细菌脂蛋白和脂多糖,以及不饱和脂肪酸。食物中后者摄取不足会激活TLR - 4和R - 2,这是病理改变的一种机制。在先天免疫受体过度激活的情况下,会出现脂肪组织炎症、细胞因子过度产生以及胰岛素抵抗。这会促进肥胖、糖尿病和动脉粥样硬化的发展。