Adam, P. A. J., Räihä, N., Rahiala, E.‐L. and Kekomäki, M. (Departments of Pediatrics, Case Western Reserve University at Cleveland Metropolitan General Hospital, Cleveland, Ohio USA, and the University of Helsinki at the Children's Hospital, Helsinki, Finland). Oxidation of glucose and D‐B‐OH‐butyrate by the early human fetal brain. Acta Paediatr Scand, 64:17, 1975.–The isolated brains of 12 previable human fetuses obtained at 12 to 21 weeks' gestation, were perfused through the interval carotid artery with glucose (3 mM) and/or DL‐B‐OH‐butyrate (DL‐BOHB), 4.5 mM, plus tracer quantities of either glucose‐6‐ 14 C (G6 14 C) or β‐OH‐butyrate‐3‐ 14 C (BOHB3 14 C). Oxidative metabolism was demonstrated by serial collection of gaseous 14 CO 2 from the closed perfusion system, and from the recirculating medium. Glucose and BOHB were utilized at physiological rates as indicated (mean ±SEM): G6 14 C at 0.10±0.01 μmoles/min g brain ( n =7) or 17.5±1.9 μmoles/ min kg fetus; and BOHB3 14 C at 0.16±0.05 μmoles/min g ( n =5) or 27.3±7.4 μmoles/ min kg. Based on fetal weight, glucose metabolism by brain apparently accounted for about 1/3 of basal glucose utilization in the fetus. On a molar basis BOHB3 14 C was taken up at 1.47 times the rate of G6 14 C. Both BOHB3 14 C and G6 14 C were converted to 14 C0 2 . The rate of BOHB3 14 C conversion to 14 CO 2 was equal to its rate of consumption, and exceeded the conversion of glucose to CO 2 because 45% of the G6 14 C was incorporated into lactate‐ 14 C. Accordingly, both substrates support oxidative metabolism by brain; and BOHB is a major potential alternate fuel which can replace glucose early in human development.
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