Interorgan glutamine flow in metabolic acidosis.
Interorgan glutamine flow in metabolic acidosis.
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代谢性酸中毒时的器官间谷氨酰胺流动。
DOI：
10.1152/ajprenal.1987.253.6.f1069
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
T. Welbourne
中科院分区：
文献类型：
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作者：
T. Welbourne
酸碱平衡取决于谷氨酰胺从生产器官流向能够产生碳酸氢盐的器官。谷氨酰胺氧化是代谢转化的先决条件，可在许多位点表达;然而，净碱基生成需要谷氨酰胺流向特定器官（肾脏）。正常情况下，谷氨酰胺从外周流到内脏床，提供主要燃料并支持尿素生成。另一方面，慢性代谢性酸中毒中的谷氨酰胺流改道至肾脏; NH+4和HCO 3-在尿液和肾静脉中的不对称分布有助于碱性储备的恢复。显然，谷氨酰胺的流动符合生理需求，但很少有人知道的调控机制。作为一个模型，慢性代谢性酸中毒改变了这一重要流动的两个方面，其方向和幅度。典型的流动方向是远离内脏床并进入与动脉谷氨酰胺浓度显著下降相关的肾脏，恢复动脉水平使血流返回内脏床水槽。因此，谷氨酰胺稳态被牺牲，以赋予方向，器官间谷氨酰胺流。虽然多个位点有助于谷氨酰胺体内平衡，但具有重要战略意义的是由肠道代谢前馈的门静脉NH+4激活的强效肝转氨酶通量;局部氢离子浓度调节该激活剂的有效性。肺可对血流方向进行急性调节，以确定主要的pCO 2和细胞酸度;慢性酸中毒的呼吸代偿可使肝谷氨酰胺酶表达，从而抑制动脉谷氨酰胺浓度。谷氨酰胺从肌肉流向肾脏的巨大幅度分别得到谷氨酰胺合成酶和线粒体谷氨酰胺酶适应性增加的支持。（250字处删节）
Acid-base homeostasis depends on glutamine flow from producer organs to those capable of generating bicarbonate. Glutamine oxidation, the prerequisite metabolic transformation, can be expressed by many sites; however, net base generation requires that glutamine flow be directed to a specific organ, the kidney. Normally, glutamine flows from the periphery to the splanchnic bed, providing a major fuel and supporting ureagenesis. Glutamine flow in chronic metabolic acidosis, on the other hand, is rerouted to the kidneys; asymmetrical distribution of NH+4 and HCO3- into the urine and renal vein subserves restoration of alkaline reserves. Clearly, glutamine flows in accordance with physiological demands, yet little is known of the regulatory mechanisms. As a model, chronic metabolic acidosis alters two aspects of this vital flow, its direction and magnitude. Characteristically the direction of flow is away from the splanchnic bed and into the kidneys associated with a marked fall in arterial glutamine concentration, restoring arterial level returns flow to the splanchnic bed sink. Thus glutamine homeostasis is sacrificed to impart direction to interorgan glutamine flow. Although multiple sites contribute to glutamine homeostasis, of great strategic importance is the potent hepatic glutaminase flux activated by portal venous NH+4 fed forward by gut metabolism; local hydrogen ion concentration modulates the effectiveness of this activator. Acute regulation of flow direction can be exerted by the lungs in determining the prevailing pCO2 and cellular acidity; respiratory compensation in chronic acidosis allows the expression of hepatic glutaminase, thereby suppressing arterial glutamine concentration. The enormous magnitude of glutamine flowing from muscle to the kidneys is supported by adaptive increases in glutamine synthetase and mitochondrial glutaminase, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)