Influence of Exogenous Glucagon on Fetal Glucose Metabolism and Ketone Production

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Abstract
Summary: Acute glucagon injections were performed in chronically catfa-eterized fetal lambs in late gestation to assess the fetal metabolic response to exogenous glucagon infusion. Glucagon dosages between 1 ug/kg and 1 mg/kg induced significant fetal hyperglycemia by 15–30 min postinjection, with peak glucose values 130–180% of control. Increasing responsivity to the same dose/kg was noted to parallel increasing gestational age. In selected preparations in which umbilical venous catheters were implanted, glucagon injection caused an acute fail in the glucose/oxygen quotient and net umbilical glucose consumption. The fall in glucose consumption to 8% of control values occurred within 15 min of injection and suggests acute fetal glucose excretion, probably secondary to hepatic ghycogenorysis. Glucagon injection in the neonatal lamb caused qualitatively similar increases in plasma glucose concentration but the quantitative responses were considerably greater. No change in fetal β-hydroxybntyrate (β-OHB) concentration was noted after injection; nor did the fetal uptake or excretion of this ketone change. The neonatal β-OHB concentration was significantly different (P < 0.001) from fetal concentrations and did rise 14% above control after glucagon injection; thus, elevation of plasma glucagon in the fetus causes an acute hyperglycemia but, unlike the adult, does not induce a significant ketogenesis. Speculation: The fetus in late gestation may respond to substrate deprivation by secretion of glucagon. If so, a modest but significant hyperglycemia would result, presumably the result of acute fetal glycogenolysis. The acute fetal metabolic adaptation to maternal starvation, however, if modified by glucagon, does not include utilization of ketones as alternate substrates.

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