Fetal and Neonatal Responses to Maternal Canine StarvationCirculating Fuels and Neonatal Glucose Production
作者:
R. KLIEGMAN,
E. MIETTINEN,
P. ADAM,
期刊:
Pediatric Research
(OVID Available online 1981)
卷期:
Volume 15,
issue 6
页码: 945-951
ISSN:0031-3998
年代: 1981
出版商: OVID
关键词: fasting;glucose;hypoglycemia;metabolism
数据来源: OVID
摘要:
Pregnant dogs were starved for 72 hr while controls were fasted overnight. Maternal starvation significantly reduced fetal birth weight (269 ± 7.2versus294 ± 4.4 g). Total caloric deprivation had no effect on maternal or fetal blood glucose concentrations 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 ± 0.39versus0.74 ± 0.2 mM) and ketone bodies (2.99 ± 0.70versus1.04 ± 0.48). Although fetal free fatty acids increased minimally (0.39 ± 0.03versus0.22 ± 0.07), ketone body levels were markedly elevated (2.53 ± 0.35versus1.01 ± 0.32). After birth, plasma-free fatty acid and β-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 ± 15versus187.6 ± 26 μM.Glucose production was significantly depressed in pups of starved mothers at 3 (13.7 ± 1.4versus22.7 ± 3) and 9 hr (17.5 ± 2.2versus26.0 ± 2.8 μmoles/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.SpeculationBecause glucose concentration and turnover were depressed whereas glucose clearance was elevated early during neonatal fasting, diminished oxidation of alternate fuels (such as fatty acids) may necessitate enhanced glucose consumption. Diminished intrahepatic oxidation of fatty acids may limit the energy source for sufficient glucose production from gluconeogenic precursors.
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