急性暴露于AICAR可增加小鼠趾长伸肌和比目鱼肌中的葡萄糖转运。
Acute exposure to AICAR increases glucose transport in mouse EDL and soleus muscle.
作者信息
Balon T W, Jasman A P
机构信息
Department of Diabetes, Endocrinology and Metabolism, Gonda Research Center, Beckman Research Institute of the City of Hope Medical Center, 1500 E. Duarte Road, California 91010, USA.
出版信息
Biochem Biophys Res Commun. 2001 Apr 13;282(4):1008-11. doi: 10.1006/bbrc.2001.4677.
AMP-activated protein kinase (AMPK) may regulate a number of metabolic processes including glucose transport. 5-Aminoimidazole-4-carboxamideribonucleoside (AICAR), an AMPK activator, has been used to study the potential role of AMPK in rat skeletal muscle; however, its effects on glucose transport in mouse skeletal muscle are unknown. Incubation with 2 mM AICAR increased 2-deoxyglucose transport in EDL muscle from both rats and mice by 86 and 37%, respectively. In contrast, AICAR did not increase 2-deoxyglucose transport in rat soleus muscle. However, AICAR induced a large (81%) increase in 2-deoxyglucose transport in soleus muscles obtained from mice. It is proposed that nonspecificity of the stimulation of glucose transport in mouse muscle may be due to a greater percentage of fast-twitch muscle fibers within the muscles.
AMP激活的蛋白激酶（AMPK）可能调节包括葡萄糖转运在内的许多代谢过程。5-氨基咪唑-4-甲酰胺核苷（AICAR）是一种AMPK激活剂，已被用于研究AMPK在大鼠骨骼肌中的潜在作用；然而，其对小鼠骨骼肌葡萄糖转运的影响尚不清楚。用2 mM AICAR孵育分别使大鼠和小鼠的EDL肌肉中的2-脱氧葡萄糖转运增加了86%和37%。相比之下，AICAR并未增加大鼠比目鱼肌中的2-脱氧葡萄糖转运。然而，AICAR使从小鼠获得的比目鱼肌中的2-脱氧葡萄糖转运大幅增加（81%）。有人提出，小鼠肌肉中葡萄糖转运刺激的非特异性可能是由于肌肉中快肌纤维的比例更高。
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