2型糖尿病与骨骼肌和其他组织的葡萄糖利用能力下降有关。胰岛素抵抗可能与遗传因素和糖尿病本身的代谢异常如高血糖或非脂化脂肪酸(NEFA)升高有关。遗传因素和继发的胰岛素抵抗代谢异常可能是由于调节葡萄糖代谢的胰岛素受体和受体后信号传导的改变引起。胰岛素与其受体结合后,受体自身磷酸化,受体激酶活化,一些细胞间的底物磷酸化,其中在骨骼肌细胞中胰岛素受体底物-1(IRS-1)最重要。酪氨酸磷酸化的IRS与脂肪激酶磷脂酚肌醇3’(PI3’)激 Type 2 diabetes is associated with decreased glucose utilization in skeletal and other tissues. Insulin resistance may be related to genetic factors and metabolic abnormalities of diabetes itself such as hyperglycemia or elevation of non-fatty fatty acids (NEFA). Genetic and secondary metabolic abnormalities in insulin resistance may be caused by altered insulin receptors that regulate glucose metabolism and post-receptor signaling. Insulin binding to its receptor, receptor autophosphorylation, receptor kinase activation, some of the intercellular substrate phosphorylation, insulin receptor substrate-1 (IRS-1) in skeletal muscle cells in the most important. Tyrosine Phosphorylated IRS Stimulates 3 ’(PI3’) Stimulation with Lipid Phospholipid Phosphatidylinositol