糖尿病肾病患者饮食中无氮类似物替代苏氨酸的可能性:生化方面

A. Malinovskiy
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摘要

有一个公认的理论认为,苏氨酸的一种必需氨基酸不能进行转氨化。根据这一理论,在患有肾病的患者的饮食中,包括糖尿病患者的苏氨酸,不会被它的酮类似物所取代。然而,苏氨酸的转氨化,特别是在人类有机体中,已经被许多研究人员发现。这表明在肾病患者的营养中有可能用其无氮类似物取代苏氨酸。同时,所有氨基酸的无氮类似物不仅可以氧化分解成最终产物,而且还可以形成葡萄糖或酮体,或两者兼而有之。根据这一点,氨基酸被分为仅产糖,仅生酮或两者同时存在。对于糖尿病来说,这一点尤为重要,因为糖原氨基酸及其无氮类似物的引入具有积极作用,而生酮氨基酸及其无氮类似物的引入是不可接受的。这是由于在转化为葡萄糖之前,糖原氨基酸被转化为克雷布斯循环的一种或另一种成分,或转化为丙酮酸,丙酮酸与刺激乙酰辅酶A氧化的成分平衡,从而刺激酮体。与糖尿病有关的酮可由两种原因引起。虽然健康人的主要能量来源是碳水化合物,但如果患有糖尿病,脂肪被强烈氧化,它们会形成大量的酮体。第二个原因是丙酮酸生成草酰乙酸(克雷布斯循环催化剂)的减少,这是由于丙酮酸从葡萄糖生成草酰乙酸的减少和克雷布斯循环成分用于糖异生的增加。由于乙酰乙酸和-羟基丁酸在血液中的积累以及第三酮体丙酮的麻醉作用,酮糖使pH值急剧转向更酸性。就糖尿病而言,致死性结果的原因是由于pH值急剧转变为更高的酸度而引起的糖尿病昏迷,这扰乱了酵素的工作。苏氨酸在完全没有生酮作用的情况下对人体有很强的生糖作用。在这方面,苏氨酸的无氮类似物与它没有区别。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The possibility of replacing threonine by nitrogen-free analogues in a diet of patients with diabetic nephropathy: a biochemical aspect
There is a well established theory that an essential amino acid of threonine is incapable of transamination. According to this theory, in a diet of patients who suffer from nephropathy, including diabetic threonine, is not replaced by its ketoanalogue. However, transamination of threonine, in the human organism in particular, has been discovered by a number of researchers. This suggests that there is a possibility of replacing threonine by its nitrogen-free analogues in nutrition of patients with nephropathy. At the same time nitrogen-free analogues of all amino acids can be subject to oxidative decomposition subsequently not only up to the finishing products, but they can also form glucose or ketone bodies, or both. Depending on this, amino acids are divided into glucogenic only, ketogenic only or both at the same time. With reference to diabetes this becomes especially important as introduction of glucogenic amino acids and their nitrogen-free analogues has a positive effect, whereas that of ketogenic amino acids and their nitrogen-free analogues is inadmissible. This is caused by the fact that before being transformed into glucose, glucogenic amino acids are transformed into one or another component of Krebs cycle or into the pyruvic acid which is in balance with the components which stimulates oxydation of acetyl coenzyme A and, therefore, ketone bodies. Ketose with reference to diabetes can be caused by two reasons. While the main source of energy of a healthy person is carbohydrate, in case with diabetes fats perform the function being oxydized intensively, they form a great number of ketone bodies. The second reason is a decrease in the formation of oxaloacetic acid (Krebs cycle catalyst) from pyruvic acid due to a decrease in the formation of the latter from glucose and an increase in the use of the components of the Krebs cycle for gluconeogenesis. Ketose causes a sharp shift of pH value to more acidity as a result of accumulation of the acetoacetic acid and the -hydroxybutyric acid in blood and narcotic actions of the third ketonic body acetone. The reason for lethal outcome with reference to diabetes is diabetic coma caused by a sharp shift of pH value to more acidity, which disturbs the work of the ferments. Threonine has a strong glucogenic effect in the complete absence of a ketogenic effect on the human body. In this respect, nitrogen-free analogues of threonine do not differ from it.
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