Ferré Pascal
INSERM, UMR S 872, Centre de Recherches des Cordeliers, Paris, France - Université Pierre et Marie Curie-Paris 6, UMR S 872, Paris, France.
Therapie. 2007 Jul-Aug;62(4):277-84. doi: 10.2515/therapie:2007052. Epub 2007 Nov 6.
Insulin controls carbohydrate and lipid metabolism. Among other things, it stimulates glucose storage as glycogen and lipid storage as triglycerides. Insulin acts through a membrane receptor which is a tyrosine kinase. When activated by insulin binding, the tyrosine kinase will recruit and phosphorylate intracellular substrates called IRS (insulin receptor substrate). Phosphorylated IRS will be used as docking sites for proteins which will transmit the insulin signal through several systems (e.g. PI3-kinase). The insulin resistance which is concomitant with type 2 diabetes and obesity is linked to an increased intracellular availability of fatty acids which are precursors of lipid mediators inducing a decreased efficiency of insulin signal transmission. Therapies aimed at improving insulin sensitivity could then target proteins involved in the regulation of intacellular fatty acid availibility.
胰岛素控制碳水化合物和脂质代谢。除此之外，它还刺激葡萄糖以糖原形式储存以及脂质以甘油三酯形式储存。胰岛素通过一种作为酪氨酸激酶的膜受体发挥作用。当被胰岛素结合激活时，酪氨酸激酶会募集并磷酸化称为IRS（胰岛素受体底物）的细胞内底物。磷酸化的IRS将作为蛋白质的停靠位点，这些蛋白质将通过多种系统（如PI3激酶）传递胰岛素信号。与2型糖尿病和肥胖症相关的胰岛素抵抗与细胞内脂肪酸可用性增加有关，脂肪酸是脂质介质的前体，会导致胰岛素信号传递效率降低。那么，旨在提高胰岛素敏感性的疗法可能会针对参与调节细胞内脂肪酸可用性的蛋白质。
