酸中毒对大鼠肝脏中由乳酸生成葡萄糖的糖异生作用的抑制机制。
The mechanism of inhibition by acidosis of gluconeogenesis from lactate in rat liver.
作者信息
Iles R A, Cohen R D, Rist A H, Baron P G
出版信息
Biochem J. 1977 Apr 15;164(1):185-91. doi: 10.1042/bj1640185.
Abstract
- Gluconeogenesis from lactate or pyruvate was studied in perfused livers from starved rats at perfusate pH7.4 or under conditions simulating uncompensated metabolic acidosis (perfusate pH6.7-6.8). 2. In 'acidotic' perfusions gluconeogenesis and uptake of lactate or pyruvate were decreased. 3. Measurement of hepatic intermediate metabolites suggested that the effect of acidosis was exerted at a stage preceding phosphoenolpyruvate. 4. Total intracellular oxaloacetate concentration was significantly decreased in the acidotic livers perfused with lactate. 5. It is suggested that decreased gluconeogenesis in acidosis is due to substrate limitation of phosphoenolypyruvate carboxykinase. 6. The possible reasons for the fall in oxaloacetate concentration in acidotic livers are discussed; two of the more likely mechanisms are inhibition of the pyruvate carboxylase system and a change in the [malate]/[oxaloacetate] ratio due to the fall in intracellular pH.
摘要
- 研究了在灌注液pH值为7.4的饥饿大鼠肝脏灌流模型中，以及在模拟未代偿代谢性酸中毒的条件下（灌注液pH值为6.7 - 6.8），乳酸或丙酮酸的糖异生作用。2. 在“酸中毒”灌流中，糖异生以及乳酸或丙酮酸的摄取减少。3. 肝脏中间代谢产物的测量表明，酸中毒的影响作用于磷酸烯醇丙酮酸之前的阶段。4. 在灌注乳酸的酸中毒肝脏中，细胞内草酰乙酸的总浓度显著降低。5. 提示酸中毒时糖异生减少是由于磷酸烯醇丙酮酸羧激酶的底物限制。6. 讨论了酸中毒肝脏中草酰乙酸浓度下降的可能原因；两个较可能的机制是丙酮酸羧化酶系统受到抑制以及由于细胞内pH值下降导致[苹果酸]/[草酰乙酸]比值发生变化。
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