Division of Endocrinology, Department of medicine, University of Colorado, Denver, USA.
Diabetol Metab Syndr. 2011 Jun 13;3(1):10. doi: 10.1186/1758-5996-3-10.
Either endogenous or exogenous hyperinsulinemia in the setting of insulin resistance promotes phosphorylation and activation of farnesyltransferase, a ubiquitous enzyme that farnesylates Ras protein. Increased availability of farnesylated Ras at the plasma membrane enhances mitogenic responsiveness of cells to various growth factors, thus contributing to progression of cancer and atherosclerosis. This effect is specific to insulin, but is not related to the type of insulin used. Stimulatory effect of hyperinsulinemia on farnesyltransferase in the presence of insulin resistance represents one potential mechanism responsible for mitogenicity and atherogenicity of insulin.
无论是内源性还是外源性的胰岛素抵抗导致的高胰岛素血症，都会促进法呢基转移酶的磷酸化和激活，法呢基转移酶是一种普遍存在的酶，可将 Ras 蛋白法尼基化。质膜中法尼基化 Ras 的可用性增加会增强细胞对各种生长因子的有丝分裂反应性，从而促进癌症和动脉粥样硬化的进展。这种作用是胰岛素特有的，与所用胰岛素的类型无关。胰岛素抵抗状态下高胰岛素血症对法尼基转移酶的刺激作用代表了胰岛素促有丝分裂和动脉粥样硬化作用的一个潜在机制。
