Inhibition of mammary gland acetyl CoA carboxylase by fatty acids

Abstract

It has been suggested that accumulation of milk in the lactating rat mammary gland following weaning may contribute toward the rapid cessation of fatty acid synthesis which ensues (Levy, 1963a; 1963b). The strong inhibition of fatty acid synthesis in rat mammary extracts produced by the addition of small quantities of rat milk provides support for this concept (Levy, 1963a; 1963b). Examination of acetyl CoA carboxylase in mammary extracts revealed that this enzyme was markedly inhibited by rat milk (Levy, 1963b). The inhibitory activity was located entirely in the residue (R 105) obtained upon centrifuging the milk at 105,000 × g; none was found in the fat layer or in the clear supernatant solution (Levy, 1963b). This communication describes attempts to elucidate the nature of the inhibitor and the mechanism of inhibition of acetyl CoA carboxylase.