Abstract
Fetal growth is inversely related to litter size. Little is known about the mechanisms responsible for this or its potential consequences in the newborn. To address this, we developed a fetal ablation model in the rat. After anesthetizing the mother on day 15 (term 21.5 days), we ligated selected arteries in the secondary cascade of uterine vessels. This ablates individual fetuses, Ablation (A) reduced fetal number compared to controls (C) (5±2 v 8±3) and accelerated fetal growth (Birthweight 5.34±.05 v 5.01±.09 g, p<.01). A pups had increased liver mass .289±.005 v .254±.005 g, p<.001) but similar liver/body ratios compared to C suggesting symmetrical growth enhancement. To some extent accelerated growth was mediated by insulin, a critical growth stimulating hormone, since plasma insulin conc were significantly elevated in A v C newborns (112.2± 14.2 v 67.0±10.1 uU/ml, p<.001). A pups developed hypoglycemia at 0 and 20 minutes of life (20 min 78.2±2.6 v 91.0±4.8 mg/dl, p<.01). This resulted from a carryover of fetal hyperinsulinism (20 min 211.2±16.0 v 52.5±19.0 uU/ml, p<.01) since plasma glucagon conc did not differ (20 min 736.7±80.0 v 655.0±99.0 pg/ml) and hepatic glycogen cone remained elevated in A pups (20 min 71.4±3.2 v 52.08±6.4 mg/g liver, p<.01). Restricting litter size may enhance blood flow to the remaining fetuses thereby enhancing metabolic fuel supply, fetal growth, and hepatic glycogen deposition. Increased insulin availability may mediate these changes and also cause neonatal hypoglycemia.
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