Modulation of leucine oxidation and turnover by graded amounts of carbohydrate intake in obese subjects.
Modulation of leucine oxidation and turnover by graded amounts of carbohydrate intake in obese subjects.
复制标题
通过肥胖受试者碳水化合物摄入量的分级来调节亮氨酸氧化和周转。
DOI：
10.1016/0026-0495(82)90096-8
复制
发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Morse,EL
中科院分区：
文献类型：
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作者：
Adibi,SA;Stanko,RT;Morse,EL
我们先前对大鼠组织的体外研究表明，酮体可能调节支链氨基酸的氧化。为了研究这一观察结果的生理和临床意义，我们确定了饥饿诱导的酮症对肥胖受试者亮氨酸代谢的影响。在饥饿前和饥饿后一周（80卡/天），测定静脉输注微量[1- 14 C]-亮氨酸后的周转率、血浆清除率和呼气14 CO2产生率（氧化指标）。这种饮食处理导致14 CO2产生率显著增加，但显著降低了亮氨酸的周转率（9.1 mmol/hr对7.0 mmol/hr）和血浆清除率（65 L/hr对34 L/hr）。当通过每天摄入300卡路里的碳水化合物来预防酮症时，14 CO2的产生率显著降低。另一方面，饥饿诱导的亮氨酸周转率和血浆清除率降低、支链氨基酸血浆浓度升高（蛋白水解增强的标志物）、丙氨酸血浆浓度降低（刺激肝再生的标志物）以及葡萄糖和胰岛素血浆浓度降低，直到碳水化合物摄入量增加到每天500或800卡路里时才能预防。每日碳水化合物摄入量的增加（高达500卡路里）伴随着尿氮排泄的减少，但不是3-甲基组氨酸（肌肉蛋白水解的标志物）。我们的数据表明：（1）酮病直接或间接地增强亮氨酸的氧化，（2）饥饿诱导的酮病、蛋白水解和蛋白质生成可以通过每天提供300-800卡路里的碳水化合物饮食依次预防，（3）饥饿时亮氨酸周转减少最可能是蛋白质合成减少的结果，（4）支链氨基酸催化剂的减少是碳水化合物的节氮效应的一个组成部分。
Our previous in vitro studies with rat tissues have suggested that ketone bodies may regulate the oxidation of branched-chain amino acids. To investigate the physiological and clinical significance of this observation, we determined the effect of starvation-induced ketosis on leucine metabolism in obese subjects. Rates of turnover, plasma clearance, and expiratory14CO2production (indicator of oxidation) after intravenous infusion of a trace amount of [1-14C]-leucine were measured before and one week after starvation (80 cal/day). This dietary treatment caused a significant increase in the rate of14CO2production, but significantly reduced the turnover (9.1 versus 7.0 mmole/hr) and plasma clearance (65 versus 34 L/hr) of leucine. When ketosis was prevented by a daily intake of 300 calories of carbohydrate, the rate of14CO2production was significantly decreased. On the other hand, starvation-induced decreases in turnover and plasma clearance of leucine, increases in plasma concentrations of branched-chain amino acids (marker for heightened proteolysis), decreases in plasma concentrations of alanine (marker for stimulated hepatic gluconeogenesis), and decreases in plasma concentrations of glucose and insulin were not prevented until carbohydrate intake was increased to 500 or 800 calories per day. Increases in daily carbohydrate intake (up to 500 calories) were accompanied by decreases in urinary excretion of nitrogen, but not 3-methylhistidine (marker for muscle proteolysis). Our data suggest that: (1) ketosis directly or indirectly enhances oxidation of leucine, (2) starvation-induced ketosis, proteolysis, and gluconeogenesis can be prevented sequentially by carbohydrate diets providing fro 300–800 calories per day, (3) the reduced turnover of leucine in starvation is most likely the result of reduced protein synthesis, and (4) diminution of branched-chain amino acid catabolism is a component of the nitrogen-sparing effect of carbohydrate.