Effects of acid-base alterations and protein depletion on hepatic nitrogen metabolism.

Effects of acid-base alterations and protein depletion on hepatic nitrogen metabolism.
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酸碱变化和蛋白质消耗对肝氮代谢的影响。

DOI:
10.1007/978-1-4615-5945-0_14
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发表时间:
1997
影响因子:
--
通讯作者:
O'Donovan,DJ
O'Donovan,DJ
中科院分区:
医学4区
文献类型:
--
作者:
Schoolwerth,AC;O'Donovan,DJ

文献摘要

相似文献

酸碱平衡的改变会对身体的许多系统产生广泛的影响。长期以来,人们一直认为酸碱调节与氮代谢有关。铵(NH4+)是正常尿液的一种成分,在代谢性酸中毒时排泄更多。早期的研究表明,酸中毒时NH4+排泄量的增加与尿素排泄率的下降是一致的。当人们意识到哺乳动物组织中缺乏尿素酶时,我们得出结论,尿素不是尿氨的直接来源。肾脏提取谷氨酰胺对尿NH4+有显著贡献,这一发现将注意力集中在肾脏谷氨酰胺的代谢上。现已证实,在慢性代谢性酸中毒中,肾脏对谷氨酰胺的提取和肾脏线粒体谷氨酰胺的脱酰胺都是加速的。
An alteration in acid-base balance has wide-ranging effects on many systems in the body. It has long been recognized that acid-base regulation is linked to nitrogen metabolism. Ammonium (NH4+), which is a constituent of normal urine, is excreted in greater quantities in metabolic acidosis. Earlier work showed that the rise in NH4+excretion in acidosis coincided with a decrease in the rate of urea excretion. When it was realized that the enzyme urease was lacking in mammalian tissues, it was concluded that urea is not a direct source of urinary NH4+. The discovery that the extraction of glutamine by the kidney contributed significantly to urinary NH4+focused attention on the renal metabolism of glutamine. It is now well established that the extraction of glutamine by the kidney and the renal mitochondrial deamidation of glutamine are accelerated in chronic metabolic acidosis.