Energy stores and intermediates of carbohydrate metabolism were investigated in the freeze-clamped cerebral cortex of the fetus and fasted neonate born to a diabetic canine mother. Prior studies in these same pups demonstrated circulating
hyperinsulinemia, depressed
free fatty acid levels, and attenuated gluconeogenesis. Hepatic and muscle tissue also demonstrated augmented levels of
glycogen,
triglycerides, and
amino acids. In the present investigation, cerebral tissue from these same pups of diabetic mothers also demonstrated enhanced fetal cerebral
glucose and
glycogen content. After 24 h of neonatal fasting, cerebral
glycogen content declined to values lower than in control pups. Cerebral cortical levels of
glucose-6-phosphate,
fructose-6-phosphate,
lactate,
citrate,
alpha-ketoglutarate, and
malate were not altered, while
oxaloacetate was higher at 3 and 9 h and
fructose-1,6-diphosphate was higher at 9 and 24 h in the IDM pups.
Adenine nucleotide levels and the energy charge were equivalent to those in control pups at each time interval. In contrast, cerebral cortical
amino acids of the
glutamate group were enhanced in the fetus or neonate of the diabetic mother. Cerebral cortical
alanine was increased from 3 to 24 h while
aspartate and
glutamate were augmented in the fetus and fasted IDM newborn pup.
Glutamine was increased at 6 and 24 h, while gamma-aminobutyrate was elevated in the fetus. Cerebral
ammonia concentration was not altered. The augmented stores of cerebral
carbohydrate and
amino acid pools in the fetus and neonate after maternal canine diabetes may serve as oxidizable substrates for the brain during periods of attenuated systemic fuel availability.(ABSTRACT TRUNCATED AT 250 WORDS)