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饥饿和糖尿病大鼠分离肝细胞中载体介导的乳酸摄取增强。

Enhanced carrier-mediated lactate entry into isolated hepatocytes from starved and diabetic rats.

作者信息

Metcalfe H K, Monson J P, Cohen R D, Padgham C

机构信息

Medical Unit, London Hospital Medical College, Whitechapel, United Kingdom.

出版信息

J Biol Chem. 1988 Dec 25;263(36):19505-9.

PMID:3198638
Abstract

Hepatic plasma membrane lactate transport was studied in isolated hepatocytes prepared from fed, starved, and streptozotocin diabetic rats. Carrier-mediated lactate entry was determined using the lactate transport inhibitors alpha-cyano-3-hydroxycinnamate and D-3-hydroxybutyrate and was significantly greater in hepatocytes from starved compared to fed rats and in hepatocytes from diabetic fed compared to fed rats. The saturable component of lactate entry which corresponds to carrier-mediated transport was higher in the starved than in the fed state with results from diabetic fed being intermediate between the two. Insulin treatment prevented the increment in carrier-mediated lactate transport observed in hepatocytes from diabetic fed rats. The data indicate that hepatic plasma membrane lactate transport is increased under conditions of starvation and diabetes mellitus. This may partly explain the increased gluconeogenic flux under these conditions.

摘要

在从喂食、饥饿和链脲佐菌素诱导的糖尿病大鼠制备的分离肝细胞中研究了肝细胞膜乳酸转运。使用乳酸转运抑制剂α-氰基-3-羟基肉桂酸酯和D-3-羟基丁酸酯测定载体介导的乳酸进入,与喂食大鼠相比,饥饿大鼠肝细胞中的载体介导的乳酸进入显著增加,与喂食大鼠相比,糖尿病喂食大鼠肝细胞中的载体介导的乳酸进入也显著增加。与载体介导的转运相对应的乳酸进入的可饱和成分在饥饿状态下高于喂食状态,糖尿病喂食大鼠的结果介于两者之间。胰岛素治疗可防止糖尿病喂食大鼠肝细胞中观察到的载体介导的乳酸转运增加。数据表明,在饥饿和糖尿病状态下,肝细胞膜乳酸转运增加。这可能部分解释了在这些条件下糖异生通量增加的原因。

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