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A possible role for malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis.丙二酰辅酶A在肝脏脂肪酸氧化和酮体生成调节中的可能作用。
J Clin Invest. 1977 Jul;60(1):265-70. doi: 10.1172/JCI108764.
2
Effect of clofibrate treatment on acylcarnitine oxidation in isolated rat liver mitochondria.氯贝丁酯治疗对分离的大鼠肝脏线粒体中酰基肉碱氧化的影响。
Med Biol. 1979 Feb;57(1):58-65.
3
Importance of experimental conditions in evaluating the malonyl-CoA sensitivity of liver carnitine acyltransferase. Studies with fed and starved rats.实验条件在评估肝脏肉碱酰基转移酶丙二酸单酰辅酶A敏感性中的重要性。对喂食和饥饿大鼠的研究。
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Hormonal regulation of ketone-body metabolism in man.人体酮体代谢的激素调节
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Inhibition by acetyl-CoA of hepatic carnitine acyltransferase and fatty acid oxidation.乙酰辅酶A对肝脏肉碱脂酰转移酶及脂肪酸氧化的抑制作用。
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Characteristics of fatty acid oxidation in rat liver homogenates and the inhibitory effect of malonyl-CoA.
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本文引用的文献

1
PALMITYL-COA:CARNITINE PALMITYLTRANSFERASE. PURIFICATION FROM CALF-LIVER MITOCHONDRIA AND SOME PROPERTIES OF THE ENZYME.棕榈酰辅酶A:肉碱棕榈酰转移酶。从小牛肝脏线粒体中纯化及该酶的一些性质
Biochim Biophys Acta. 1964 Jul 8;89:95-108.
2
Carbohydrate sparing of fatty acid oxidation. I. The relation of fatty acid chain length to the degree of sparing. II. The mechanism by which carbohydrate spares the oxidation of palmitic acid.脂肪酸氧化的碳水化合物节约作用。I. 脂肪酸链长度与节约程度的关系。II. 碳水化合物节约棕榈酸氧化的机制。
Arch Biochem Biophys. 1955 Jul;57(1):23-40. doi: 10.1016/0003-9861(55)90173-9.
3
The regulation of ketogenesis from octanoic acid. The role of the tricarboxylic acid cycle and fatty acid synthesis.辛酸生酮作用的调节。三羧酸循环和脂肪酸合成的作用。
J Biol Chem. 1971 Feb 25;246(4):1149-59.
4
Ketone body metabolism in the ketosis of starvation and alloxan diabetes.饥饿性酮症和四氧嘧啶糖尿病中酮体的代谢
J Biol Chem. 1970 Sep 10;245(17):4382-90.
5
The regulation of ketogenesis from oleic acid and the influence of antiketogenic agents.油酸生酮作用的调节及抗生酮剂的影响。
J Biol Chem. 1971 Oct 25;246(20):6247-53.
6
The effects of starvation and refeeding on carbohydrate and lipid metabolism in vivo and in the perfused rat liver. The relationship between fatty acid oxidation and esterification in the regulation of ketogenesis.饥饿和再喂养对大鼠体内及灌注肝脏中碳水化合物和脂质代谢的影响。脂肪酸氧化与酯化在生酮调节中的关系。
J Biol Chem. 1973 Jan 10;248(1):270-8.
7
The concentration of malonyl-coenzyme A and the control of fatty acid synthesis in vivo.丙二酰辅酶A的浓度与体内脂肪酸合成的调控
J Biol Chem. 1972 Nov 25;247(22):7325-31.
8
Comparison of properties of carnitine palmitoyltransferase I with those of carnitine palmitoyltransferase II, and preparation of antibodies to carnitine palmitoyltransferases.
J Biol Chem. 1973 Jun 10;248(11):4069-74.
9
Hormonal control of ketogenesis. Rapid activation of hepatic ketogenic capacity in fed rats by anti-insulin serum and glucagon.生酮作用的激素调控。抗胰岛素血清和胰高血糖素对喂食大鼠肝脏生酮能力的快速激活。
J Clin Invest. 1975 Jun;55(6):1202-9. doi: 10.1172/JCI108038.
10
Role of carnitine in hepatic ketogenesis.肉碱在肝脏生酮作用中的角色。
Proc Natl Acad Sci U S A. 1975 Nov;72(11):4385-8. doi: 10.1073/pnas.72.11.4385.

丙二酰辅酶A在肝脏脂肪酸氧化和酮体生成调节中的可能作用。

A possible role for malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis.

作者信息

McGarry J D, Mannaerts G P, Foster D W

出版信息

J Clin Invest. 1977 Jul;60(1):265-70. doi: 10.1172/JCI108764.

DOI:10.1172/JCI108764
PMID:874089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC372365/
Abstract

Studied on the oxidation of oleic and octanoic acids to ketone bodies were carried out in homogenates and in mitochondrial fractions of livers taken from fed and fasted rats. Malonyl-CoA inhibited ketogenesis from the former but not from the latter substrate. The site of inhibition appeared to be the carnitine acyltransferase I reaction. The effect was specific and easily reversible. Inhibitory concentrations were in the range of values obtained in livers from fed rats by others. It is proposed that malonyl-CoA functions as both precursor for fatty acid synthesis and suppressor of fatty acid oxidation. As such, it might be an important element in the carbohydrate-induced sparing of fatty acid oxidation.

摘要

在取自喂食和禁食大鼠的肝脏匀浆和线粒体组分中,对油酸和辛酸氧化生成酮体进行了研究。丙二酸单酰辅酶A抑制前者生成酮体,但不抑制后者底物生成酮体。抑制位点似乎是肉碱脂酰转移酶I反应。该效应具有特异性且易于逆转。抑制浓度在其他研究者从喂食大鼠肝脏中获得的值范围内。有人提出,丙二酸单酰辅酶A既是脂肪酸合成的前体,又是脂肪酸氧化的抑制剂。因此,它可能是碳水化合物诱导的脂肪酸氧化节约现象中的一个重要因素。