Kissebah A H, Tulloch B R, Hope-Gill H, Clarke P V, Vydelingum N, Fraser T R
Lancet. 1975 Jan 18;1(7899):144-7. doi: 10.1016/s0140-6736(75)91435-x.
A unifying hypothesis is proposed for the mechanism of insulin action in adipose tissue. Insulin both induces displacement of Ca++ from a membrane-bound pool and inhibits efflux of the ion, thereby facilitating a rise in intracellular free Ca++ concentration. The former effect could enhance the transport of substrates and ions into the cell, while the latter modulates the activity of some intracellular enzymes to stimulate glycogenesis, lipogenesis, and decrease lipolysis and glycogenolysis. The calcium ion might act as the missing second messenger for insulin action.
针对胰岛素在脂肪组织中的作用机制提出了一个统一的假说。胰岛素既能诱导钙离子从膜结合池中置换出来,又能抑制离子外流,从而促进细胞内游离钙离子浓度升高。前一种效应可增强底物和离子进入细胞的转运,而后一种效应则调节某些细胞内酶的活性,以刺激糖原合成、脂肪生成,并减少脂肪分解和糖原分解。钙离子可能是胰岛素作用中缺失的第二信使。