METABOLIC FUEL UTILIZATION AND PYRUVATE OXIDATION DURING THE POSTNATAL-PERIOD

The transplacental supply of nutrients is interrupted at birth, which diverts maternal metabolism to lactation, After birth, energy hameosta sis is rapidly regained through milk nutrients which supply the newbor n with the fatty acids and ketone bodies required for neonatal develop ment. However, immediately after birth and before the onset of sucklin g there is a time lapse in which the newborn undergoes a unique kind o f starvation. During this period glucose is scarce and ketone bodies a re not available owing to the delay in ketogenesis. Under these circum stances, the newborn is supplied with another metabolic fuel, lactate, which is utilized as a source of energy and carbon skeletons. Neonata l rat lung, heart, liver and brain utilize lactate for energy producti on and lipogenesis. Lactate is also utilized by the brain of human bab ies with type I glycogenosis. Both rat neurons and astrocytes in prima ry culture actively use lactate as an oxidizable substrate and as a pr ecursor of phospholipids and sterols. Lactate oxidation is enhanced by dichloroacetate, an inhibitor of the pyruvate dehydrogenase kinase in neurons bur not in astrocytes, suggesting that the pyruvate dehydroge nase is regulated differently in each type of cell. Despite the low ac tivity of this enzyme in newborn brain, pyruvate decarboxylation is th e main fate of glucose in both neurons and astrocytes. The occurrence of a yeast-like pyruvate decarboxylase activity in neonatal brain may explain these results.