Adult Diabetes Program, University of Colorado Denver, Mail Stop 8106, 12631 E 17th Ave, Aurora, CO 80045, USA.
Diabetologia. 2010 Feb;53(2):229-33. doi: 10.1007/s00125-009-1558-6. Epub 2009 Oct 23.
Either endogenous or exogenous hyperinsulinaemia in the setting of insulin resistance promotes phosphorylation and activation of farnesyltransferase, a ubiquitous enzyme that farnesylates Ras proteins. 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. The stimulatory effect of hyperinsulinaemia 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引起的高胰岛素血症，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，增强了细胞对各种生长因子的有丝分裂反应性，从而促进了癌症和动脉粥样硬化的发展。这种作用是胰岛素特有的，但与所用胰岛素的类型无关。在胰岛素抵抗存在的情况下，高胰岛素血症对法呢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。
