MEDIUM-CHAIN FATTY-ACIDS AS SHORT-TERM REGULATORS OF HEPATIC LIPOGENESIS
MEDIUM-CHAIN FATTY-ACIDS AS SHORT-TERM REGULATORS OF HEPATIC LIPOGENESIS
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DOI：
10.1042/bj3020141
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发表时间：
1994-08-15
影响因子：
4.1
通讯作者：
GEELEN, MJH
中科院分区：
文献类型：
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作者：
GEELEN, MJH
短期暴露于短链和中链脂肪酸导致乙酰辅酶A羧化酶的激活，如在毛地黄皂苷透化肝细胞中所测量的。达到一定浓度，典型的每种脂肪酸使用，脂肪酸依赖性激活乙酰辅酶A羧化酶与脂肪酸合成率在完整的肝细胞中的增加相一致，通过从（H2O）-H-3水的H-3掺入脂肪酸。在较高的浓度下，脂肪酸合成的刺激损失发生，但不是羧化酶活性的增强。对于测试的脂肪酸（C-8：0-C-14：0），脂肪酸合成的峰与丙二酰辅酶A水平的峰一致。羧化酶活性的刺激的开始与脂肪酸合成和丙二酰辅酶A的峰值的开始一致。添加的脂肪酸的链长越长，脂肪酸合成速率和丙二酰辅酶A水平达到峰值时的浓度越低，羧化酶活性开始升高。在细胞悬浮液中培养的脂肪酸浓度增加，积累的乳酸逐渐减少。后一个观察结果，结合乙酰辅酶A羧化酶的活性并不总是与脂肪酸生物合成速率相关的事实，表明在这些条件下，不是羧化酶的活性，而是通过糖酵解序列的通量至少部分地决定了脂肪酸从头合成的速率。
Short-term exposure of isolated rat hepatocytes to short- and medium-chain fatty acids led to an activation of acetyl-CoA carboxylase as measured in digitonin-permeabilized hepatocytes. Up to a certain concentration, typical for each of the fatty acids used, fatty acid-dependent activation of acetyl-CoA carboxylase coincided with an increase in the rate of fatty acid synthesis in intact hepatocytes, as determined by the incorporation of H-3 from (H2O)-H-3 water into fatty acids. At higher concentrations loss of stimulation of fatty acid synthesis occurred, but not the enhancement of carboxylase activity. With the fatty acids tested (C-8:0-C-14:0), the peak in fatty acid synthesis coincided with a peak in the level of malonyl-CoA. The onset of the stimulation of carboxylase activity coincided with the start of the peak in both fatty acid synthesis and malonyl-CoA. The longer the chain length of the fatty acid added, the lower the concentration at which the rate of fatty acid synthesis and the level of malonyl-CoA reached a peak and carboxylase activity started to become elevated. In cell suspensions incubated with increasing concentrations of fatty acids, accumulation of lactate decreased progressively. The latter observation, in combination with the fact that the activity of acetyl-CoA carboxylase is not always related to the rate of fatty acid biosynthesis, suggests that under these conditions not the activity of the carboxylase but the flux through the glycolytic sequence determines, at least in part, the rate of fatty acid synthesis de novo.