Hay W W, Meznarich H K
Q J Exp Physiol. 1986 Oct;71(4):689-98. doi: 10.1113/expphysiol.1986.sp003027.
In order to measure the effect of hyperinsulinaemia on fetal glucose metabolism and oxygen consumption, we applied the glucose-clamp technique to experiments in fifteen late-gestation, unstressed, chronically catheterized fetal lambs. In a control period, and immediately thereafter following 2 h of hyperinsulinaemia, we measured fetal glucose utilization and oxidation rates (radioactive tracer methodology) and net fetal uptake rates of exogenous glucose and oxygen uptake rates (Fick principle). During the period of hyperinsulinaemia, fetal glucose concentration was maintained at the average control period value by a variable rate of glucose infusion into the fetus in response to serial 10 min measurements of fetal arterial blood glucose concentration. Hyperinsulinaemia in the fetus (12.12 +/- 1.92 ng X ml-1 (mean +/- S.E.M.) arterial plasma) resulted in a 13% increase in net fetal oxygen uptake rate (0.310 +/- 0.011 to 0.349 +/- 0.012 mmol. min-1 X kg-1), a 106% increase of fetal glucose uptake rate (4.54 +/- 0.43 to 9.35 +/- 0.50 mg X min-1 X kg-1) and an 83% increase of fetal glucose utilization rate (4.94 +/- 0.43 to 9.05 +/- 0.83 mg X min-1 X kg-1). Fetal glucose uptake and utilization rates were not different from each other during the control and the hyperinsulinaemia periods. The fraction of glucose that was oxidized (0.58 +/- 0.05, control; 0.54 +/- 0.05, hyperinsulinaemia) did not change significantly; thus the glucose oxidation rate, the rate of entry of glucose into non-oxidative pathways, and the amount of oxygen used for glucose oxidation all increased in proportion to glucose utilization. These results suggest that insulin promotes the entry of glucose into fetal tissues, thereby increasing fetal glucose utilization and oxidation rates and substituting glucose oxidation for that of other substrates. The insulin-enhanced glucose utilization rate also increases slightly fetal metabolic rate.
为了测定高胰岛素血症对胎儿葡萄糖代谢和氧消耗的影响，我们将葡萄糖钳夹技术应用于15只妊娠晚期、未受应激、长期插管的胎羊实验。在对照期以及随后高胰岛素血症持续2小时后，我们测量了胎儿葡萄糖利用和氧化速率（放射性示踪法）以及胎儿对外源性葡萄糖的净摄取率和氧摄取率（菲克原理）。在高胰岛素血症期间，根据对胎儿动脉血葡萄糖浓度进行的连续10分钟测量结果，通过向胎儿输注可变速率的葡萄糖，将胎儿葡萄糖浓度维持在对照期的平均水平。胎儿高胰岛素血症（动脉血浆中胰岛素浓度为12.12±1.92 ng·ml-1（平均值±标准误））导致胎儿净氧摄取率增加13%（从0.310±0.011增至0.349±0.012 mmol·min-1·kg-1），胎儿葡萄糖摄取率增加106%（从4.54±0.43增至9.35±0.50 mg·min-1·kg-1），胎儿葡萄糖利用率增加83%（从4.94±0.43增至9.05±0.83 mg·min-1·kg-1）。在对照期和高胰岛素血症期，胎儿葡萄糖摄取率和利用率没有差异。被氧化的葡萄糖比例（对照期为0.58±0.05，高胰岛素血症期为0.54±0.05）没有显著变化；因此，葡萄糖氧化速率、葡萄糖进入非氧化途径的速率以及用于葡萄糖氧化的氧量均与葡萄糖利用率成比例增加。这些结果表明，胰岛素促进葡萄糖进入胎儿组织，从而提高胎儿葡萄糖利用和氧化速率，并以葡萄糖氧化替代其他底物的氧化。胰岛素增强的葡萄糖利用率也使胎儿代谢率略有增加。
