Abstract
ABSTRACT: We used chronic fetal glucose infusion to test the hypothesis that chronic fetal hyperglycemia and hyperinsulinemia inhibit the development of β-receptor binding capapcity (Bmax) in fetal lamb lung. Glucose was infused (14 ± 4 mg/kg/h, mean ± SD) into eight twin and four singleton fetuses from 112 days gestation until death between 118–145 days gestation. The other eight twins and eleven additional singleton fetuses served as controls. Serum glucose levels were elevated 2-fold and serum insulin levels were elevated 3-fold in the glucose-infused fetuses. In the control fetuses β-receptor Bmax increased 2.5-fold between 130 days gestation and term. However, this increase was attenuated to 1.5-fold in the glucose infused fetuses, p < 0.01. The 50% inhibition of Bmax was similar in both male and female fetuses, except that the Bmax fell to 30% lower levels in males, p < 0.01. Chronic glucose infusion also resulted in an 80% reduction in lung lavage saturated phosphatidylcholine content, and an 85% reduction in tracheal fluid saturated phosphatidylcholine content, p < 0.001. Lung lavage and tracheal fluid saturated phosphatidylcholine content correlated significantly with beta receptor Bmax (r = 0.9, r = 0.85). We conclude that chronic glucose infusion inhibits the development of β-receptor binding in fetal lamb lung, and that this effect is greater in males than females. Such a mechanism could be a factor in the predisposition of infants of diabetic mothers to develop respiratory distress and could contribute to a male disadvantage in respiratory morbidity.
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Warburton, D., Buckley, S., Parton, L. et al. Chronic Glucose Infusion Inhibits Development of β-Receptor Binding in Fetal Lamb Lung. Pediatr Res 24, 171–174 (1988). https://doi.org/10.1203/00006450-198808000-00006
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DOI: https://doi.org/10.1203/00006450-198808000-00006