The overall objective of this project is to define the pathophysiologic mechanisms involved in neonatal hypoglycemia, especially that seen in the small-for-gestational-age (SGA) newborn. We are studying metabolic fuel and hormonal responses to the initial extra-uterine fasting, with particular emphasis on the availability of alternate fuels (beta-hydroxybutyrate, acetoacetate, and free fatty acids), the availability of substrate for gluconeogenesis (lactate, pyruvate, and alanine), and the hormonal milieu. Since our preliminary studies indicate that the rat model does not resemble what is seen in the human neonate, pilot studies have been undertaken to see whether the guinea pig can serve as a useful model for neonatal hypoglycemia. BIBLIOGRAPHIC REFERENCES: Stanley, C., and Baker, L.: Hyperinsulinism in Infancy: Diagnosis by Demonstration of Abnormal Response to Fasting Hypoglycemia. Ped. 57:702, 1976. Ranke, M.B., Stanley, C., Rodbard, D., Baker, L., Bongiovanni, A., and Parks, J.: Sex differences in Binding of Human G with Hormone to Isolated Rat Hepatocytes. Proc. Nat. Acad. Sci. USA 73:847, 1976.