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在糖尿病大鼠的灌注肝脏中,由L-丙氨酸生成肝葡萄糖的过程不存在。

Hepatic glucose production from L-alanine is absent in perfused liver of diabetic rats.

作者信息

Ferraz M, Brunaldi K, Oliveira C E, Bazotte R B

机构信息

University Paranaense, Umuarama, PR, Brazil.

出版信息

Res Commun Mol Pathol Pharmacol. 1997 Feb;95(2):147-55.

PMID:9090751
Abstract

The effects of L-alanine on hepatic glucose production in diabetic rats and the corresponding controls was investigated. Diabetes was obtained with an injection iv of streptozotocin (STZ) or alloxan. Livers from diabetic and control rats after 24 hours of fasting were perfused in situ and glucose production from L-alanine and several gluconeogenic substrates were measured. Hepatic gluconeogenesis from L-alanine was absent in rats with diabetes induced by STZ or alloxan. STZ-diabetic rats also shown this metabolic change when the period of diabetes was prolonged. It was concluded that this effect may be partly at least, the consequence of an increased NADH/NAD+ ratio in the diabetic rat liver, which indicates that the cytosolic redox potential is favorable to pyruvate conversion to L-lactate but not to glucose. However, considering that glucose production from pyruvate, L-lactate, glycerol and sorbitol was not affected by the diabetic condition, the rate of conversion of L-alanine to pyruvate can contribute to the lack of gluconeogenesis when this amino acid was employed as a substrate.

摘要

研究了L-丙氨酸对糖尿病大鼠及相应对照组肝脏葡萄糖生成的影响。通过静脉注射链脲佐菌素(STZ)或四氧嘧啶诱导糖尿病。禁食24小时后的糖尿病大鼠和对照大鼠的肝脏进行原位灌注,并测量L-丙氨酸和几种糖异生底物的葡萄糖生成情况。由STZ或四氧嘧啶诱导的糖尿病大鼠肝脏中不存在由L-丙氨酸生成葡萄糖的糖异生过程。当糖尿病病程延长时,STZ诱导的糖尿病大鼠也表现出这种代谢变化。得出的结论是,这种效应至少部分可能是糖尿病大鼠肝脏中NADH/NAD⁺比值升高的结果,这表明胞质氧化还原电位有利于丙酮酸转化为L-乳酸,而不利于转化为葡萄糖。然而,考虑到丙酮酸、L-乳酸、甘油和山梨醇的葡萄糖生成不受糖尿病状态的影响,当使用这种氨基酸作为底物时,L-丙氨酸向丙酮酸的转化率可能导致糖异生缺乏。

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