ACETOGENESIS DOES NOT REPLACE KETOGENESIS IN FASTING PIGLETS INFUSED WITH HEXANOATE

The current studies were performed to better understand the physiologi cal relevance of acetate in the poorly ketogenic piglet and to determi ne if endogenous acetogenesis rises with increased mitochondrial fatty acid P-oxidation, analogous to ketogenesis. Plasma acetate concentrat ion values in newborn, fasted, or suckled piglets (230-343 mu M) were at least 10-fold higher than the ketone bodies, a pattern opposite to that in 24- to 48-h suckled rats (77-175 mu M). Employing continuous i nfusion techniques with sodium [H-3]acetate tracer in fasting similar to 40-h-old piglets, acetate rate of appearance (R-a) was found to be 34 +/- 4 mu mol.min(-1).kg body wt(-1). This basal R-a was double that observed in animals coinfused with sodium [1-C-14]hexanoate (P < 0.00 1), despite active oxidation of the latter as determined by (CO2)-C-14 production. Active acetogenesis in vivo and relatively abundant aceta te in piglet blood are consistent with the hypothesis that acetate pla ys an important physiological role in piglets. However, the negative i mpact of hexanoate oxidation upon acetate R-a and the lack of signific ant changes in circulating acetate in newborn, suckled, and fasted pig lets draws into question the extent of analogy between acetogenesis an d ketogenesis in vivo.