Abstract
The development of two urea cycle enzymes, carbamylphosphate synthetase-I and ornithine transcarbamylase was examined in neonatal rat liver. Normal birth on day 21.5 caused a marked increase of both activities as early as 4 h of extrauterine life. That increase occurred later in newborns delivered by cesarian section on day 21.5, but they exhibited a greater hepatic urea level. Premature delivery on day 20.5 caused a marked increase of both activities and hepatic urea level while prolonged gestation abolished these increases. The postnatal increase in both activities and in hepatic urea level was therefore dependent on a factor associated with birth. The in vivo administration of actinomycin D (2 μg) at birth did not abolish the postnatal increase of both activities. Moreover, the administration of glucose (25 mg every 2 h) to newborns delivered by cesarian section on day 21.5 abolished the postnatal increase of ornithine transcarbamylase activity and hepatic urea level 23 h later. It seems that the transient hypoglycemia and appearance of gluconeogenesis at birth were the physiological mechanisms involved in the postnatal induction of ornithine transcarbamylase activity.
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