Abstract

Newborn rats,starved from birth develop between 12 and 16h a profound hypoglycemia due to a deficient gluconeogenesis.The lack of lipid stores results in a low rate of hepatic fatty acid oxidation which has been proposed as the rate limiting factor in gluconeogenesis.When 13h old starved rats are fed with M.C.T,blood glucose increases,in 3h,from 1.30 ± 0.09mM to 4.23 ± 0.23mM.This results from a stimulation of glucose production (63H glucose) from 3.9 ± 0.5mg/min/kg to 11.1 ± 0.6mg/min/kg due to a 5-fold increased gluconeogenesis.Despite their utilization for glucose synthesis, blood levels of lactate,alanine and pyruvate are increased 2 to 3-fold after M.C.T feeding. When M.C.T feeding is given in association with dichloroacetate (an activator of pyruvate dehydrogenase-(P-D.H)) there is no increase in blood lactate,alanine and pyruvate levels and the increase in glycemia is prevented.This suggests that hyperketonemia due to M.C.T feeding could decrease the oxidation of 3 carbons glucose precursors in peripheral tissues secondary to an inhibition of P.D.H and thus enhances their release in blood. These studies demonstrate that M.C.T feeding stimulates glucose production in the newborn rat,both,by increasing the availability of gluconeogenic precursors and by a direct effect on hepatic gluconeogenesis.

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