Pregnant dogs were starved for 72 hr while controls were fasted overnight. Maternal starvation significantly reduced fetal birth weight (269 +/- 7.2 versus 294 +/- 4.4 g). Total caloric deprivation had no effect on maternal or fetal blood glucose concentration at the time of delivery; however, fasting neonatal blood glucose levels were depressed during the first 9 hr of life. Starvation produced a large elevation of maternal free fatty acids (1.68 +/- 0.39 versus 0.74 +/- 0.2 mM) and ketone bodies (2.99 +/- 0.70 versus 1.04 +/- 0.48). Although fetal free fatty acids increased minimally (0.39 +/- 0.03 versus 0.22 +/- 0.07), ketone body levels were markedly elevated (2.53 +/- 0.35 versus 1.01 +/- 0.32). After birth, plasma-free fatty acid and beta-hydroxybutyrate levels were lower in pups of starved mothers at 3 hr, and acetoacetate was lower at 6 and 9 hr. Other alternate fuels such as amino acids demonstrated lower levels of glutamine in pups of starved mothers throughout the day (except 3 hr), whereas alanine levels declined significantly only at 24 hr (114.9 +/- 15 versus 187.6 +/- 26 microM. Glucose production was significantly depressed in pups of starved mothers at 3 (13.7 +/- 1.4 versus 22.7 +/- 3) and 9 hr (17.5 +/- 2.2 versus 26.0 +/- 2.8 mumoles/kg/min), whereas glucose clearance rates were elevated at 3, 6 and 9 hr of age. Lactate carbon incorporation into glucose increased throughout the day but was not significantly affected by prior maternal starvation.
Heptic glycolytic and gluconeogenic intermediates from fasted newborns of five control and five 3-day starved canine mothers (MCS) were studied at 0, 3, 6, 9, and 24 h of age. MCS did not affect fetal hepatic glycogen concentration; however, a significant increase in uridine diphosphate glucose (UDPG) (0.186 vs. 0.106 mumol/g), fructose 6-phosphate (0.084 vs. 0.034), pyruvate (0.321 vs. 0.126), and citrate (0.190 vs. 0.140) concentrations occurred. At 3 h, the intrahepatic glucose concentration among the MCS newborns declined (3.09 vs. 6.34) and remained lower than the controls for up to 9 h. UDPG concentration, however, remained elevated throughout the 24 h. In addition intrahepatic pyruvate was significantly elevated in the MCS group. Elevated phosphoenolpyruvate concentrations were observed between 3 and 6 h. Malate levels were lower than controls between 6 and 9 h and alpha-ketoglutarate was significantly higher between 6 and 24 h. Calculated cytoplasmic NAD/NADH ratio was elevated throughout the 24 h. Hepatic triglycerides were higher than controls up to 9 h. A decline in hepatic triglycerides was observed between 9 and 24 h. The results suggest increased glycolysis and suppressed gluconeogenesis in the MCS puppies, probably because of increased triglyceride synthesis and decreased free fatty acid oxidation resulting in a lack of cytoplasmic NADH.
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