The control of mitochondrial beta-oxidation, including the delivery of acyl moieties from the plasma membrane to the mitochondrion, is reviewed. Control of beta-oxidation flux appears to be largely at the level of entry of acyl groups to mitochondria, but is also dependent on substrate supply. CPTI has much of the control of hepatic beta-oxidation flux, and probably exerts high control in intact muscle because of the high concentration of malonyl-CoA in vivo. beta-Oxidation flux can also be controlled by the redox state of NAD/NADH and ETF/ETFH(2). Control by [acetyl-CoA]/[CoASH] may also be significant, but it is probably via export of acyl groups by carnitine acylcarnitine translocase and CPT II rather than via accumulation of 3-ketoacyl-CoA esters. The sharing of control between CPTI and other enzymes allows for flexible regulation of metabolism and the ability to rapidly adapt beta-oxidation flux to differing requirements in different tissues.

中文翻译：

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线粒体β-氧化通量的控制。

审查了线粒体β-氧化的控制，包括从质膜到线粒体的酰基部分的传递。β-氧化通量的控制似乎主要在酰基进入线粒体的水平上，但也取决于底物的供应。CPTI对肝脏的β-氧化通量有很大的控制作用，并且由于体内丙二酰辅酶A的浓度高，CPTI可能对完整的肌肉发挥了很大的控制作用。β-氧化通量还可以通过NAD / NADH和ETF / ETFH（2）的氧化还原状态进行控制。[乙酰基-CoA] / [CoASH]的控制也可能很重要，但可能是通过肉碱酰基肉碱转位酶和CPT II出口酰基，而不是通过3-酮酰基-CoA酯的积累。