Acute exposure to AICAR increases glucose transport in mouse EDL and soleus muscle |
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Authors: | Balon T W Jasman A P |
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Affiliation: | 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. tbalon@coh.org |
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Abstract: | 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. |
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