Hepatic acetogenesis and ketogenesis in neonatal swine

[摘要] Reports of low circulating ketone bodies ($\beta$-hydroxybutyrate, $\beta$-OHB & acetoacetate) in suckling piglets and evidence of minimal hepatic ketone body production from fatty acids in vitro suggested that, unlike previously-studied neonates, enhanced ketogenesis does not characterize the metabolism of the newborn pig. This apparent idiosyncracy of piglet metabolism prompted a series of studies examining development and regulation of ketogenesis in piglets, and the physiological implications of low ketonemia in piglets. The extent of alternative pathways (non-ketogenic routes of carbon flux into Krebs cycle intermediates, e.g.) of fatty acid $\beta$-oxidation was also assessed. Low ketogenic capacity in piglets was confirmed by the small change in plasma ($\beta$-OHB) relative to (C8:0) (regression slope) following a dose of C8:0. This slope was 1-2 orders of magnitude lower vs. that of mature pigs and newborn or mature rabbits. Minimal fatty acid carboxyl-carbon accumulated in ketone bodies after incubations of piglet liver homogenates or hepatocytes with (1-$\sp{14}$C) -C7:0, -C8:0, or -C16:0 in vitro, consistent with the in vivo results. The observed low activity of the ketogenic enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (HMG-CoA synthase) increased plasma (insulin) with suckling (patterns opposite that seen in ketotic neonatal rats, e.g.) may in part explain attenuated ketogenic capacity in piglets. Piglets accumulated fatty acid carboxyl-carbon in acetate to a high degree relative to ketone bodies in incubations of liver tissue with radiolabeled fatty acids, a phenomenon previously unreported for any animal. It is thus speculated that acetate plays a more important physiological role than the ketone bodies in newborn piglets, an idea supported by the small contribution of ketone bodies to the energy budget of piglets ($

[效力级别] Health Sciences, Nutrition

[关键词] Biology, Animal Physiology;Health Sciences, Nutrition