Silverman M S, Mynarcik D C, Corin R E, Haspel H C, Sonenberg M
Memorial Sloan-Kettering Cancer Center, Cornell University Medical College, New York, New York 10021.
Endocrinology. 1989 Nov;125(5):2600-4. doi: 10.1210/endo-125-5-2600.
We have studied the effects of GH on basal and insulin-stimulated hexose transport by 3T3-F442A adipocytes in a hormonally defined serum-free medium. Adipocytes preincubated in defined medium exhibit a low level of hexose transport which is acutely (15 min) stimulated (greater than 5-fold) by insulin (EC50, 0.1-0.2 nM). GH has acute (15-45 min) insulin-mimetic (greater than 2-fold) and chronic (4-48 h) diabetogenic (50-80%) effects on basal and insulin-stimulated hexose transport. The insulin-mimetic effect of GH has a higher EC50 (2 nM) than its diabetogenic effect (EC50, 0.2 nM). Chronic GH exposure decreases the maximal responsiveness (50-80%) and the acute sensitivity (approximately 2-fold) of hexose transport to insulin. Insulin-stimulated transport is more (approximately 5-fold) sensitive to the diabetogenic effect of GH than is basal transport. Insulin binding and degradation were not altered by chronic exposure to GH. The diabetogenic effect of GH may occur at a postinsulin binding level.
我们在一种激素限定的无血清培养基中研究了生长激素(GH)对3T3 - F442A脂肪细胞基础和胰岛素刺激的己糖转运的影响。在限定培养基中预孵育的脂肪细胞表现出低水平的己糖转运,胰岛素(EC50,0.1 - 0.2 nM)可使其急性(15分钟)刺激(超过5倍)。GH对基础和胰岛素刺激的己糖转运具有急性(15 - 45分钟)胰岛素模拟(超过2倍)和慢性(4 - 48小时)致糖尿病(50 - 80%)作用。GH的胰岛素模拟作用的EC50(2 nM)高于其致糖尿病作用的EC50(0.2 nM)。长期暴露于GH会降低己糖转运对胰岛素的最大反应性(50 - 80%)和急性敏感性(约2倍)。胰岛素刺激的转运比基础转运对GH的致糖尿病作用更敏感(约5倍)。长期暴露于GH不会改变胰岛素结合和降解。GH的致糖尿病作用可能发生在胰岛素结合后的水平。