Abstract
Synthesis of glucose from non-carbohydrate precursors has been considered to be absent in fetal liver of many mammals, with post-natal appearance of gluconeogenesis subject to hormonal regulation. Using a new method for perfusion of fetal liver and isolation of hepatocytes, the development of gluconeogenesis in the rat fetus was investigated.
Fetal hepatocytes, isolated following in situ perfusion with collagenase, actively converted both alanine and pyruvate to glucose during the day prior to normal delivery. Glucose production in isolated hepatocytes was linear for at least two hours and was proportional to substrate concentration. Both glucagon (.014 to 1.4 uM) and oleic acid (.0064 to .64 uM) markedly enhanced conversion of both alanine and pyruvate to glucose; the effect of both was directly proportional to the basal rate of gluconeogenesis. Neither insulin nor b-OH butyrate inhibited glucagon or oleic acid enhancement of glucose production. Preincubation of fetal hepatocytes (21 day fetus) with glucagon effected a maximal increase in gluconeogenic rates.
These studies indicate that gluconeogenesis is initiated in isolated hepatocytes derived from the rat fetus just prior to term. Regulation of gluconeogenesis by hormones or fatty acids is proportional to basal rates of glucose production. Assuming no marked changes in endogenous glucagon or insulin secretion, initiation of gluconeogenesis during fetal development does not appear to be hormonally determined.
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Greenberg, R., Howell, W. 858 INITIATION OF GLUCONEOGENESIS DURING FETAL DEVELOPMENT. Pediatr Res 12 (Suppl 4), 506 (1978). https://doi.org/10.1203/00006450-197804001-00863
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DOI: https://doi.org/10.1203/00006450-197804001-00863