Wolf George
Department of Nutritional Sciences and Toxicology, University of California, Berkeley, California, USA.
Nutr Rev. 2007 May;65(5):251-6. doi: 10.1111/j.1753-4887.2007.tb00302.x.
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.
胰岛素抵抗发生在肥胖、代谢综合征和2型糖尿病的情况下。研究发现，它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减少导致脂肪细胞分泌血清视黄醇结合蛋白RBP4。血清RBP4水平升高似乎是实验动物和人类全身性胰岛素抵抗发展的信号。在小鼠中，血清RBP4水平升高导致骨骼肌葡萄糖摄取受损和肝脏葡萄糖生成增加，而血清RBP4水平降低则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一种联系：RBP4，即脂肪细胞分泌到循环中的维生素A转运蛋白。
