Regulation of Placental Glucose Transfer and Consumption by Fetal Glucose Production

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Abstract
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, pppppppa 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.

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