Insulin resistance occurs under conditions of obesity, metabolic syndrome, and type 2 diabetes. It was found to be accompanied by down-regulation of the insulin-responsive glucose transporter GLUT4. Decreased adipocyte GLUT4 caused secretion by adipocytes of the serum retinol-binding protein RBP4. Enhanced levels of serum RBP4 appeared to be the signal for the development of systemic insulin resistance both in experimental animals and in humans. In mice, increased levels of serum RBP4 led to impaired glucose uptake into skeletal muscle and increased glucose production by liver, whereas lowered serum RBP4 levels greatly enhanced insulin sensitivity. Thus, a link has been established between obesity and insulin resistance: RBP4, the vitamin A-transport protein secreted into the circulation by adipocytes.

译文

胰岛素抵抗在肥胖,代谢综合症和2型糖尿病的情况下发生。发现伴随着胰岛素反应性葡萄糖转运蛋白GLUT4的下调。脂肪细胞GLUT4的减少导致脂肪细胞分泌视黄醇结合蛋白RBP4。血清RBP4水平升高似乎是实验动物和人类体内系统性胰岛素抵抗发展的信号。在小鼠中,血清RBP4水平升高会导致葡萄糖吸收到骨骼肌中,并增加肝脏产生的葡萄糖,而降低血清RBP4水平会大大增强胰岛素敏感性。因此,肥胖与胰岛素抵抗之间建立了联系:RBP4,脂肪细胞分泌到循环中的维生素A转运蛋白。

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