Effects of fetal insulin infusion on glucose kinetics in pregnant sheep: a compartmental analysis.
Effects of fetal insulin infusion on glucose kinetics in pregnant sheep: a compartmental analysis.
复制标题
胎儿胰岛素输注对怀孕绵羊葡萄糖动力学的影响：区室分析。
DOI：
10.1152/ajpendo.1986.251.4.e448
复制
发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Sperling,MA
中科院分区：
文献类型：
--
作者：
Bloch,CA;Banach,W;Landt,K;Devaskar,S;Sperling,MA
应用由胎儿（F）、子宫胎盘和母体（M）组成的三室模型定量研究了胎儿高胰岛素血症对妊娠晚期妊娠绵羊葡萄糖动力学的影响。该方法将Fick原理与差异标记的葡萄糖同位素的同位素稀释相结合，同时输注F [U-14 C]-和M [2- 3 H]葡萄糖。在基础状态下，脐带葡萄糖摄取率（8.37 +/- 0.98 mg/kg/min）和胎儿葡萄糖利用率（7.38 +/- 1.13）相当（平均值+/- SE; n = 12）。当胎儿胰岛素从13.7 +/- 2.2增加到约100 microU/ml的平台时，动脉葡萄糖从18.9 +/- 0.8下降到约13 mg/dl的新稳态（P <0.001）。90 min时脐葡萄糖摄取增加，此后保持升高（P <0.01），而60 min时胎儿葡萄糖利用仅短暂增加1.9 +/- 0.8 mg/kg/min（26%; P <0.05），然后恢复至基线。然而，胰岛素的持续作用从葡萄糖清除率从39.3 +/- 5.9至66.6 +/- 10.5 ml/kg/min的持续加倍（P <0.005）中显而易见。在整个实验过程中，没有明显的内源性胎儿葡萄糖产生。母体葡萄糖的产生和利用保持不变，尽管M葡萄糖浓度略有下降，从M到子宫胎盘和F的葡萄糖转移增加，60分钟时从33.9 +/- 8.1至48.1 +/- 7.0 mg/min（配对分析P <0.01）。我们的结论是，胎儿高胰岛素血症最初通过短暂增加胎儿对葡萄糖的利用来降低葡萄糖浓度。（250字处删节）
A three-compartment model, consisting of fetus (F), uteroplacenta, and mother (M) was applied to quantitate the effects of fetal hyperinsulinemia on glucose kinetics in pregnant sheep late in gestation. The approach combines the Fick principle with isotope dilution of differentially labeled glucose isotopes, infused simultaneously to F [U-14C]- and M [2-3H]glucose. In the basal state, rates of umbilical glucose uptake (8.37 +/- 0.98 mg/kg per min) and fetal glucose utilization (7.38 +/- 1.13) were equivalent (mean +/- SE; n = 12). When fetal insulin was increased from 13.7 +/- 2.2 to a plateau of approximately 100 microU/ml, arterial glucose decreased from 18.9 +/- 0.8 to a new steady state of approximately 13 mg/dl (P less than 0.001). Whereas umbilical glucose uptake increased at 90 min and remained elevated thereafter (P less than 0.01), fetal glucose utilization increased only transiently at 60 min by 1.9 +/- 0.8 mg/kg per min (26%; P less than 0.05) and then returned to base line. Insulin's persistent effect, however, was evident from the sustained doubling of the glucose clearance rate from 39.3 +/- 5.9 to 66.6 +/- 10.5 ml/kg per min (P less than 0.005). No endogenous fetal glucose production was evident throughout the experiments. Maternal glucose production and utilization remained unchanged, although there was a small decline in M glucose concentration and an increase in glucose transfer from M to the uteroplacenta and F, from 33.9 +/- 8.1 to 48.1 +/- 7.0 mg/min at 60 min (P less than 0.01 by paired analysis). We conclude that fetal hyperinsulinemia initially lowers glucose concentration by transiently increasing fetal glucose utilization.(ABSTRACT TRUNCATED AT 250 WORDS)