Sh. Adams et J. Odle, ACETOGENESIS DOES NOT REPLACE KETOGENESIS IN FASTING PIGLETS INFUSED WITH HEXANOATE, American journal of physiology: endocrinology and metabolism, 37(6), 1998, pp. 963-970
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.