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在失代偿期肝硬化中,骨骼肌对支链氨基酸的利用增加,尤其与氨解毒有关。

Augmented utilization of branched-chain amino acids by skeletal muscle in decompensated liver cirrhosis in special relation to ammonia detoxication.

作者信息

Hayashi M, Ohnishi H, Kawade Y, Muto Y, Takahashi Y

出版信息

Gastroenterol Jpn. 1981;16(1):64-70. doi: 10.1007/BF02820426.

DOI:10.1007/BF02820426
PMID:7227760
Abstract

Femoral arterio-venous (A-V) differences of blood free amino acids and plasma ammonia (NH3) were simultaneously determined after an overnight fast in 16 patients with decompensated liver cirrhosis in the absence and presence of encephalopathy, as compared with those in 8 control subjects. In spite of increased releases of phenylalanine (Phe) and tyrosine (Tyr) from the peripheral tissue, releases of isoleucine (Ile) and leucine (Leu) as well as alanine (Ala) were found to be significantly reduced in decompensated liver cirrhosis, particularly in the presence of hepatic encephalopathy. Furthermore, NH3 was found to be significantly taken up by the skeletal muscle of these patients, and a positive correlation was observed between arterial NH3 level and the A-V differences of Leu, of Ile and of Ala. These findings strongly suggest that net degradation (or utilization) of branched-chain amino acids (in particular, Leu and Ile) is enhanced in the muscle for detoxication of ammonia (i.e., glutamine synthesis) by supplying the carbon skeleton and energy in cirrhosis of the liver.

摘要

在16例失代偿期肝硬化患者禁食过夜后,无论有无肝性脑病,同时测定其股动静脉血中游离氨基酸和血浆氨(NH₃)的差异,并与8例对照者进行比较。尽管外周组织中苯丙氨酸(Phe)和酪氨酸(Tyr)的释放增加,但在失代偿期肝硬化患者中,尤其是存在肝性脑病时,异亮氨酸(Ile)、亮氨酸(Leu)以及丙氨酸(Ala)的释放显著减少。此外,发现这些患者的骨骼肌显著摄取NH₃,并且动脉血NH₃水平与Leu、Ile和Ala的动静脉差异之间存在正相关。这些发现强烈提示,在肝硬化时,通过提供碳骨架和能量,肌肉中支链氨基酸(特别是Leu和Ile)的净降解(或利用)增强,以促进氨的解毒(即谷氨酰胺合成)。

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