Chronic hypoglycemia was produced in pregnant rats during the last third of gestation through the constant infusion of insulin by a subcutaneously implanted, osmotically driven minipump. The offspring, delivered by cesarean section on day 20 of gestation, demonstrated intrauterine growth retardation compared to control fetuses. This effect was associated with fetal hypoglycemia and hypoinsulinemia. Fetal total and branch-chain amino acid concentrations were not affected. Increases in maternal to fetal glucose ratio and fetal insulin to glucose ratio in the experimental group were interpreted to indicate that limitation in the availability of glucose, a major fetal nutrient, was the basis for these effects.

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