Abstract
Although glucose is considered the sole metabolic fuel utilized by the fetus to meet its energy requirrements, induction of ketone-oxidizing enzymes in fetal brain tissue has recently been demonstrated in experimental animals fasted during pregnancy. The significance of such enzyme induction to fetal fuel economy is dependent ultimately on substrate availability. To examine the latter during caloric deprivation in human pregnancy, 14 physically healthy pregnant women (PW) undergoing theraputic abortion for pychiatric reasons during week 16–22 of gestation and 6 non-pregnant women (NP) were fasted for 84 hours. In PW, blood β-OH-butyrate and acetoacetate rose to 4.2 and 0.9 mM/L respectively, and were 2–3 fold higher than in NP for the first 60 hours of the fast. Throughout the fast plasma glucose was significantly lower (P < .005) in PW falling to 47 ± 1 mg%, 25% below NP levels. Maternal ketonemia and hypoglycemia influenced fetal substrate levels as reflected in amniotic fluid obtained at termination of the fast and from 11 additional non-fasted PW. Ketone acid levels in amniotic fluid increased 30–40 fold in fasted Pw to levels comparable to maternal blood (4–5 ,M/L); glucose levels in amniotic fluid in fasted PW (21 ± 1 mg%) were 40% below those in non-fasted PW (P < .001). In contrast, free fatty acid levels in amniotic fluid were not consistently increased by starvation though markedly elevated in maternal plasma. Conclusions: Pregnancy accelerates and exaggerates the ketogenic and hypoglycemic response to starvation. Increased ketone availability to the conceptus suggests that ketones become an important metabolic fuel for the fetus during maternal caloric deprivation.
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Kim, Y., Lynch, V., Felig, P. et al. Fetal-maternal metabolic fuel adaptations to caloric deprivation in human pregnancy. Pediatr Res 5, 413–414 (1971). https://doi.org/10.1203/00006450-197108000-00177
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DOI: https://doi.org/10.1203/00006450-197108000-00177