Ontko J A, Johns M L
Biochem J. 1980 Dec 15;192(3):959-62. doi: 10.1042/bj1920959.
Palmitate oxidation by liver mitochondria from fed and starved rats exhibited markedly different sensitivities to inhibition by malonyl-CoA. In the mitochondrial system from fed rats, 50% inhibition required 19 muM-malonyl-CoA, whereas the mitochondria from starved rats were by comparison refractory to malonyl-CoA. Inhibition by malonyl-CoA was completely reversed by increasing the molar ratio of fatty acid to albumin. Results indicate that the potential effectiveness of malonyl-CoA as an inhibitor of fatty acid oxidation in the liver is dependent on an unidentified regulatory component of the system. The functional activity of this component is modified by the nutritional state, and its site of action is at the mitochondrial level.
喂食和饥饿大鼠肝脏线粒体对棕榈酸的氧化作用对丙二酸单酰辅酶A的抑制表现出明显不同的敏感性。在喂食大鼠的线粒体系统中,50%的抑制需要19μM的丙二酸单酰辅酶A,而相比之下,饥饿大鼠的线粒体对丙二酸单酰辅酶A不敏感。增加脂肪酸与白蛋白的摩尔比可完全逆转丙二酸单酰辅酶A的抑制作用。结果表明,丙二酸单酰辅酶A作为肝脏脂肪酸氧化抑制剂的潜在有效性取决于该系统中一个未知的调节成分。该成分的功能活性受营养状态的影响,其作用位点在线粒体水平。