DiGiacomo J E, Hay W W
Department of Pediatrics, University of Colorado School of Medicine, Denver 80262.
Pediatr Res. 1989 May;25(5):429-34. doi: 10.1203/00006450-198905000-00001.
We studied ten normoglycemic [maternal glucose (GA) = 70 mg/dL] and six insulin-induced hypoglycemic (GA = 22 mg/dL) pregnant sheep to test the hypothesis that development of fetal glucose production (GPR) could help maintain fetal glucose concentration, limit uteroplacental-fetal glucose transfer (UPGT), and sustain uteroplacental glucose consumption (UPGC). Compared with the normoglycemic group, the hypoglycemic group demonstrated the following values: fetal glucose concentration (Ga) was 9.8 +/- 0.8 mg/dL (51% lower, p less than 0.01), uterine glucose uptake (UtGU) was 16.7 +/- 1.4 mg/min (54% lower, p less than 0.01), UPGT was 3.1 +/- 0.6 mg/min (81% lower, p less than 0.001), and UPGC was 13.6 +/- 1.4 mg/min (30% lower, p less than 0.05). The reduction in UPGC was significantly less (p less than 0.05) than the reductions in UPGT and UtGU. Fetal glucose utilization rate (GUR) was decreased 20% (p less than 0.05) to 3.99 +/- 0.35 mg/min/kg. A further decrease in GUR was prevented by the appearance of fetal GPR of 2.82 +/- 0.32 mg/min/kg (p less than 0.05) compared with negligible GPR in the normoglycemic group. UPGT and UPGC in both groups were not influenced by maternal or fetal insulin infusions as long as Ga did not change; however, fetal glucose infusion that increased Ga increased UPGC in both groups. We conclude that, during chronic maternal hypoglycemia, increased fetal GPR limits the simultaneous decrease in fetal GUR and glucose concentration. By sustaining Ga fetal GPR limits UPGT to a significantly greater extent than UtGU, diverting UtGU to UPGC. Thus, fetal GPR promotes placental as well as fetal metabolic autonomy when the maternal supply of glucose is reduced.
我们研究了10只血糖正常（母体葡萄糖[GA]=70mg/dL）和6只胰岛素诱导低血糖（GA=22mg/dL）的妊娠绵羊，以验证胎儿葡萄糖生成（GPR）的发展有助于维持胎儿葡萄糖浓度、限制子宫胎盘-胎儿葡萄糖转运（UPGT）并维持子宫胎盘葡萄糖消耗（UPGC）这一假说。与血糖正常组相比，低血糖组呈现以下数值：胎儿葡萄糖浓度（Ga）为9.8±0.8mg/dL（降低51%，p<0.01），子宫葡萄糖摄取（UtGU）为16.7±1.4mg/min（降低54%，p<0.01），UPGT为3.1±0.6mg/min（降低81%，p<0.001），UPGC为13.6±1.4mg/min（降低30%，p<0.05）。UPGC的降低明显小于UPGT和UtGU的降低（p<0.05）。胎儿葡萄糖利用率（GUR）降低20%（p<0.05）至3.99±0.35mg/min/kg。与血糖正常组中可忽略不计的GPR相比，胎儿GPR为2.82±0.32mg/min/kg（p<0.05），从而防止了GUR的进一步降低。只要Ga不变，两组的UPGT和UPGC均不受母体或胎儿胰岛素输注的影响；然而，增加Ga的胎儿葡萄糖输注会增加两组的UPGC。我们得出结论，在母体慢性低血糖期间，胎儿GPR增加可限制胎儿GUR和葡萄糖浓度的同时降低。通过维持Ga，胎儿GPR对UPGT的限制程度明显大于对UtGU的限制，将UtGU转向UPGC。因此，当母体葡萄糖供应减少时，胎儿GPR促进胎盘以及胎儿的代谢自主性。
