Toyoda N, Murata K, Sugiyama Y
Endocrinology. 1985 Mar;116(3):998-1002. doi: 10.1210/endo-116-3-998.
To elucidate the mechanism of insulin resistance during late pregnancy, we studied [125I]iodoinsulin binding, [1-14C]glucose oxidation, and 3-O-[methyl-14C]glucose transport in adipocytes isolated from pregnant rats on day 19 or 20 of gestation. Neither the affinity or number of insulin receptors on pregnant rat adipocytes differed from those on age-matched nonpregnant female rats. Insulin-stimulated glucose oxidation was reduced in the pregnant rat adipocytes. The maximum velocity of insulin-stimulated methylglucose transport was also significantly reduced in the pregnant rat adipocytes. These results suggest that insulin resistance in isolated adipocytes from pregnant rats near term is caused by some postreceptor changes, one of which is a reduction in the number and/or mobility of insulin-stimulated hexose transporters.
为阐明妊娠晚期胰岛素抵抗的机制,我们研究了妊娠第19或20天从妊娠大鼠分离的脂肪细胞中[125I]碘胰岛素结合、[1-14C]葡萄糖氧化及3-O-[甲基-14C]葡萄糖转运情况。妊娠大鼠脂肪细胞上胰岛素受体的亲和力或数量与年龄匹配的未妊娠雌性大鼠的胰岛素受体并无差异。妊娠大鼠脂肪细胞中胰岛素刺激的葡萄糖氧化减少。妊娠大鼠脂肪细胞中胰岛素刺激的甲基葡萄糖转运的最大速度也显著降低。这些结果表明,妊娠晚期大鼠分离的脂肪细胞中的胰岛素抵抗是由某些受体后变化引起的,其中之一是胰岛素刺激的己糖转运蛋白数量和/或活性降低。