关于进食状态下未孕大鼠和泌乳大鼠肝细胞中脂肪生成与酮体生成之间相互关系的证据。
Evidence for a reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed virgin and lactating rats.
作者信息
Benito M, Williamson D H
出版信息
Biochem J. 1978 Oct 15;176(1):331-4. doi: 10.1042/bj1760331.
Abstract
Lipogenesis is increased in hepatocytes from fed lactating rats compared with virgin rats. Inhibition of lipogenesis with 5-(tetradecyloxy)-2-furoic acid resulted in increased ketogenesis from endogenous substrate, but not from oleate. Dihydroxyacetone increased ketogenesis from endogenous substrate, but not from oleate. Dihydroxyacetone increased lipogenesis and esterification of [1--14C]oleate and decreased ketogenesis; these changes were reversed by the inhibitor. The reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed rats may be due to alterations in [malonyl-CoA] [McGarry, Mannaerts & Foster (1977) J. Clin. Invest. 60, 265--270; Cook, King & Veech (1978) J. Biol. Chem. 253, 2529--2531], but this mechanism is not considered to be sufficient to explain the increased ketogenesis in starvation completely.
摘要
与未生育的大鼠相比，处于哺乳期且已进食的大鼠肝细胞中的脂肪生成增加。用5-（十四烷氧基）-2-呋喃甲酸抑制脂肪生成会导致内源性底物的生酮作用增加，但油酸不会。二羟基丙酮会增加内源性底物的生酮作用，但油酸不会。二羟基丙酮增加了脂肪生成以及[1-14C]油酸的酯化作用，并降低了生酮作用；这些变化可被抑制剂逆转。进食大鼠肝细胞中脂肪生成和生酮作用之间的相互关系可能是由于[丙二酰辅酶A]的改变[麦加里、曼纳茨和福斯特（1977年）《临床研究杂志》60卷，265 - 270页；库克、金和维奇（1978年）《生物化学杂志》253卷，2529 - 2531页]，但这种机制被认为不足以完全解释饥饿状态下生酮作用的增加。
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Regulation of hepatic lipogenesis by plasma free fatty acids: simultaneous studies on lipoprotein secretion, cholesterol synthesis, ketogenesis and gluconeogenesis.血浆游离脂肪酸对肝脏脂肪生成的调节：脂蛋白分泌、胆固醇合成、酮体生成及糖异生的同步研究
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