Effect of respiratory acidosis on glucose homeostasis in experimental intrauterine growth retardation in rats

Abstract

Hypoglycemia and asphyxia account for a significant proportion of morbidity in the infant with intrauterine growth retardation (IUGR). The purpose of this study was to evaluate changes in glucose homeostasis in IUGR rats during acute respiratory acidosis. IUGR was produced by bilateral uterine artery ligation at 17 days of gestation in 14 pregnant rats with 23 successfully delivered pups. The normal pups ( n = 31) were those whose mothers were sham operated at the same gestational period. The IUGR and normal pups were studied at 2 days of age. One group of pups was studied under room air while another was subjected to 20 min of exposure to a gas mixture of 10% O 2/15% CO 2, balanced with N 2. Gluconeogenesis in the liver and carcass, as well as plasma glucose and catecholamines were determined before and after the exposure to the gas mixture. The results showed that the 2-day-old IUGR rats have lower body weight (P < 0.001), liver weight (P < 0.001), plasma glucose (P < 0.001), and rate of gluconeogenesis (P < 0.01) when compared with the normally grown rats. During respiratory acidosis, the normally grown rats showed an increase in plasma epinephrine (P < 0.005) without significant change in plasma glucose and rate of gluconeogenesis. The IUGR rats on the other hand, demonstrated a decrease in rate of gluconeogenesis (P < 0.02), an increase in plasma glucose (P < 0.001) while the plasma epinephrine level remained unchanged. We speculate that respiratory acidosis blunted cellular metabolism in the IUGR rat resulting in decreased peripheral glucose utilization.