Fetal glucogenesis
Tracer studies in humans68 and sheep10 have shown that when glucose tracer is infused into the mother the specific activity or enrichment ratio of tracer (labeled) glucose to non-labeled glucose in the fetal plasma is the same as in the maternal plasma. This demonstrates that the only source of glucose in the fetus is from the maternal plasma, otherwise, new glucose production into the fetal plasma from either the fetus itself or from the placenta would dilute the tracer glucose coming from the mother along with unlabeled glucose, thus lowering the fetal enrichment ratio. Furthermore, studies in fetal sheep have shown that the net uptake of glucose by the fetus from the placenta invariably is equal to the fetal glucose utilization rate, independently measured with glucose tracers.69 Thus, there is no evidence for fetal glucose production under normal conditions. Also, there is little if any fetal glucogenesis under the conditions of short-term (1-4 h) changes in maternal and fetal glucose concentrations, the placental-to-fetal glucose transfer, and fetal glucose utilization rates. Measurable rates of fetal glucose production only develop significantly after prolonged periods (several days) of decreased fetal glucose supply, and sustained fetal hypoglycemia and hypoinsulinemia. The capacity of the fetus to make new glucose molecules from non-glucose substrates (e.g. lactate, amino acids, and glycerol)
varies considerably among species. In nearly all cases this appears to be a late gestational development, augmented by cortisol activation of phosphoenolpyruvate carboxykinase, the rate-limiting step for gluconeogenesis, and glucose-6-phosphatase, the enzyme necessary for release of glucose from the liver into the circulation.70
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