HYPOGLYCEMIA,HYPOALANIEMIA, AND KETONEMIA IN THE FASTED POSTNATAL RAT PUP: LONG-TERM CONSEQUENCES OF INTRAUTERINE GROWTH RETARDATION

Abstract

To determine the long-term metabolic consequences of intrauterine growth retardation, we fasted rat pups who were growth retarded due to bilateral maternal uterine artery ligation (L) at 3, 4, and 5 weeks of age. Pups of sham (S) and nonoperated (N) mothers were controls since birthweight differed significantly between groups. L pups had significantly reduced body and carcass mass throughout the 5 weeks. At 3 weeks, 48 hours fast reduced plasma glucose in L pups (L 78.4±5; S 89±4; N 88±2 mg/dl; p<.01). Insulin decreased (L 12.2±.2; S 25.9±.5; N 22.5±.2μU/ml; p<.01) and glucagon increased (L 862±100; S 538±65; N 539±96 pg/ml; p<.01) appropriately. Hepatic phos-phoenolpyruvate carboxykinase activity (L .55±.02; S .59±.02; N .58±.02μmoles PEP/g liver/min) and glycogen content did not differ. L pups did have significantly reduced plasma alanine (L .14±.02; S .22±.02; N .22±.02μmoles/ml; p<.05) and elevated betahydroxybutyrate (L 1.178±.90; S .799±.090; N .812±.094 μmoles/ml; p<.01). No difference in response to fasting occurred at 4 or 5 weeks. Limited gluconeogenic substrate availability may be responsible for hypoglycemia in the fasted 3 week L pup. This may represent a mechanism to spare already limited carcass protein. These metabolic alterations resemble ketotic hypoglycemia of infancy, a disorder often associated with intrauterine growth retardation.

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