Abstract
With maternal diabetes in pregnancy, the fetus receives a surfeit of metabolic fuels and as a consequence increases insulin secretion. Insulin stimulates the growth of specific tissues and the combination of increased fuels and insulin causes macrosomia. To assess the effect of hyperinsullniom alone upon the fetus, we injected fetal rats in situ with insulin (I) or saline (S) on day 18 (term 21.5 days). One day following injection, I and S fetuses were of similar weight. Fetal/maternal glucose ratios did not differ between I and S fetuses (.63-.75); however I fetuses had elevated plasma insulin (543.3±74.9 v 139.0±27.0 uU/ml, p .01) and diminished glucagon conc (151.8±24.9 v 267.7±35.0 pg/ml. By day 20, I>S fetuses (4.58±.09 v 3.16±.07g, p<.001). Insulin (165.8±19.6 v 181.2±24 uU/ml) and glucagon were equivalent between I and S fetuses. Newborn I pups weighed 5.21±.05 and S, 4.93±.09g (p<.001). While initially normoglycemic (0-60 min), I pups developed hypoglycemia at 120 and 240 min of life. This resulted from a sustained insulin effect since while S newborns decreased plasma insulin, I pups had relatively elevated values at 60, 120, and 240 min (60 min I 46.8±3.8 v 22.7±3.7 uU/ml, p<.01) and plasma glucagon did not differ (60 min 429.6±50.2 v 359.3±32 pg/ml). For these reasons, hepatic glycogen conc in I pups remained elevated (20 min 54.9±6.0 v 36.4±6.25 mg/g liver, p.<01). Insulin can stimulate fetal growth without the provision of extra fuels. Fetal hyperinsulinism is associated with delay in the normal decrease in insulin during the neonatal period and causes hypoglycemia.
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Finley, S., Ogata, E. EXOGENOUS INSULIN ACCELERATES FETAL GROWTH AND CAUSES NEONATAL HYPOGLYCEMIA IN THE RAT. Pediatr Res 21 (Suppl 4), 341 (1987). https://doi.org/10.1203/00006450-198704010-01043
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DOI: https://doi.org/10.1203/00006450-198704010-01043