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腺苷受体介导胰岛素和大鼠骨骼肌收缩对葡萄糖摄取及转运的协同刺激作用。

Adenosine receptors mediate synergistic stimulation of glucose uptake and transport by insulin and by contractions in rat skeletal muscle.

作者信息

Vergauwen L, Hespel P, Richter E A

机构信息

Exercise Physiology Laboratory, Faculty of Physical Education and Physiotherapy, Catholic University of Leuven, Belgium.

出版信息

J Clin Invest. 1994 Mar;93(3):974-81. doi: 10.1172/JCI117104.

DOI:10.1172/JCI117104
PMID:8132783
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC294012/
Abstract

The role of adenosine receptors in the regulation of muscle glucose uptake by insulin and contractions was studied in isolated rat hindquarters that were perfused with a standard medium containing no insulin or a submaximal concentration of 100 microU/ml. Adenosine receptor antagonism was induced by caffeine or 8-cyclopentyl-1,3-dipropylxantine (CPDPX). Glucose uptake and transport were measured before and during 30 min of electrically induced muscle contractions. Caffeine nor CPDPX affected glucose uptake in resting hindquarters. In contrast, the contraction-induced increase in muscle glucose uptake was inhibited by 30-50% by caffeine, as well as by CPDPX, resulting in a 20-25% decrease in the absolute rate of glucose uptake during contractions, compared with control values. This inhibition was independent of the rate of perfusate flow and only occurred in hindquarters perfused with insulin added to the medium. Thus, adenosine receptor antagonism inhibited glucose uptake during simultaneous exposure to insulin and contractions only. Accordingly, caffeine inhibited 3-O-methylglucose uptake during contractions only in oxidative muscle fibers that are characterized by a high sensitivity to insulin. In conclusion, the present data demonstrate A1 receptors to regulate insulin-mediated glucose transport in contracting skeletal muscle. The findings provide evidence that stimulation of sarcolemmic adenosine receptors during contractions is involved in the synergistic stimulation of muscle glucose transport by insulin and by contractions.

摘要

在分离的大鼠后肢中研究了腺苷受体在胰岛素和收缩调节肌肉葡萄糖摄取中的作用,这些后肢用不含胰岛素或含100微单位/毫升次最大浓度胰岛素的标准培养基灌注。咖啡因或8-环戊基-1,3-二丙基黄嘌呤(CPDPX)可诱导腺苷受体拮抗作用。在电诱导肌肉收缩30分钟之前和期间测量葡萄糖摄取和转运。咖啡因和CPDPX均不影响静息后肢的葡萄糖摄取。相反,咖啡因以及CPDPX可使收缩诱导的肌肉葡萄糖摄取增加受到30%-50%的抑制,与对照值相比,导致收缩期间葡萄糖摄取的绝对速率降低20%-25%。这种抑制与灌注液流速无关,且仅发生在向培养基中添加胰岛素灌注的后肢中。因此,腺苷受体拮抗作用仅在同时暴露于胰岛素和收缩时抑制葡萄糖摄取。相应地,咖啡因仅在对胰岛素高度敏感的氧化肌纤维的收缩过程中抑制3-O-甲基葡萄糖摄取。总之,目前的数据表明A1受体可调节收缩骨骼肌中胰岛素介导的葡萄糖转运。这些发现提供了证据,表明收缩过程中肌膜腺苷受体的刺激参与了胰岛素和收缩对肌肉葡萄糖转运的协同刺激作用。

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