Contribution of Hepatic Fatty Acid Oxidation and Exogenous Galactose Supply to the Regulation of Glucose Homeostasis in the Newborn Rabbit

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Abstract
The inhibition of hepatic gluconeogenesis by 3-mercaptopicolinic acid (3-MPA) leads to a profound hypoglycemia in both suckling and fasting 24-hour-old rabbits. This hypoglycemia is totally reversed 1 h after the intragastric injection of an amount of galactose corresponding to the one ingested daily by the suckling newborns. This results from an active gluconeogenesis from galactose, which bypasses the site of inhibition by 3-MPA. However, this amount of galactose is not sufficient to maintain a normal blood glucose concentration for a long time, since 3 h after galactose injection, the blood glucose concentrations of newborn rabbits return to hypoglycemic values. When hepatic fatty acid oxidation is inhibited by 2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate (POCA), 24-hour-old fasting rabbits become rapidly hypoglycemic secondary to a decrease in liver gluconeogenesis. The rate of hepatic gluconeogenesis is totally restored by giving medium-chain triglycerides, and the 24-hour-old rabbits become normoglycemic.