Factors Affecting Ketogenesis from Butyric Acid in the Ruminant

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Abstract
Hltraruminal infusion of butyrate at ap- proximate rates of either 8 or )6 mmole/ kg/24 hr to goats for 60 hr under varying degrees of fasting resulted in similar minor accumulations of blood ketone bodies. Un- der these conditions, no difference in the metabolism of butyrate was noted, whether it was administered as the free acid or at a pit of 6.5. Markedly increased ketone body accumulation resulted from increased rates of butyric acid infusion in goats with phlorizin-induced hypoglycemia. In- travenous glucose, intravenous propionate, or intraruminal propionate were equally effective in largely suppressing ketogenesis from butyric acid in the phlorizinized goat. The most marked ketogenesis from butyrate occurred when administered intrarumiually to fasted goats in late pregnancy. Intra- ruminal propionic acid, when superimposed on the butyric acid infusion, essentially eliminated the ketone body accumulation in this condition. Elevated plasma nonesteri- fled fatty acids during fasting were lowered when marked ketone body accumulation occurred, even when no butyric acid was administered. The evidence for a feedback mechanism for control of ketogenesis is discussed. The intermediary metabolism of butyric acid, produced by ruminal fermentation, has been studied extensively both in vitro and in vivo. In vitro conversion to ketone bodies of this acid in both tureen epithelial tissue and liver slices has been shown to be appreciable and approaches the order of 50% of the butyrate metabolized (17, 19, 26, 32). Studies conducted with iso- topically labeled butyric acid in vivo have indi- cated a significant incorporation of the label into glueogen~c materials, although most agree