HEPATIC ACETONE BODY PRODUCTION IN THE DOG DURING FASTING AND FAT FEEDING

Abstract
In post-absorptive angiostom-ized dogs no liberation of acetone bodies by the liver could be detected. During fasting or fat feeding, acetone body formation accounted for as much as 50% (av. 17%) of the total energy consumption. Urinary acetone bodies did not exceed 1.6% of the calculated daily formation. The adm. of glucose inhibited hepatic ketogenesis within 11/2 hrs. During fasting, the hepatic output of glucose decreased as that of acetone bodies increased and the total energy output as glucose plus acetone bodies remained constant. There must be 2 alternative routes for fat oxidation, one of which does not involve hepatic ketogenesis; acetone body production by the liver may be a mechanism for supplying from fat partially oxidized C compounds that can in part replace glucose in body metabolism.