Possible mechanisms by which the degree of acetylation of hepatic CoA might be regulated were examined in lactating and in non-lactating dairy cows. This involved the measurement of the hepatic steady-state concentrations of free CoA, acetyl-CoA, free carnitine, acetylcarnitine and total acid-soluble carnitine in freezeclamped biopsy samples, the measurement of the hepatic release of acetate from acetylcarnitine in vitro, and the measurement of the rate of hepatic output of acetate and ketone bodies in vivo.
The hepatic ratio of [free CoA]/[acetyl-CoA] was 0·11 in lactating cows and 0·59 in non-lactating cows. There was a significant rise in the hepatic concentration of acetyl-CoA and a significant fall in that of total acid-soluble carnitine in the lactating cows as compared with the non-lactating cows.
There was a net in vivo output of acetate and of ketone bodies from the livers of both lactating and non-lactating cows. The rates of output amounted to 7·77 and 2·00 mmole/min for acetate and ketone bodies respectively in the lactating cows, and 4·95 and 2·14 mmole/min in the non-lactating cows.
The rate of enzymic release of acetate from acetylcarnitine in vitro amounted to 0·93 and 0·34 μmole min−1 (g wet wt)−1 at 37 °C for liver homogenates derived from lactating and non-lactating cows respectively. The activity observed in the case of the lactating cows was sufficient to account for the rate of hepatic acetate output observed in vivo.