Author:
Bonen A.,Tan M. H.,Watson-Wright W. M.
Abstract
To elucidate the mechanism of enhanced insulin sensitivity by muscle after exercise, we studied insulin binding, 2-deoxy-D-[1-14C]glucose (2-DOG) uptake and [5-3H]glucose utilization in glycolysis and glycogenesis in soleus and extensor digitorum longus (EDL) muscles of mice after 60 min of treadmill exercise. In the soleus, glycogenesis was increased after exercise (P < 0.05) and remained sensitive to the action of insulin. Postexercise insulin-stimulated glycolysis was also increased in the soleus (P < 0.05). In the EDL, glycogenesis was increased after exercise (P < 0.05). However, this was already maximal in the absence of insulin and was not further stimulated by insulin (0.1–4 nM). The disposal of glucose occurred primarily via the glycolytic pathway (>60%) in the soleus and EDL at rest and after exercise. The uptake of 2-DOG uptake was not altered in the soleus after exercise (4 h incubation at 18 °C). However, with 1-h incubations at 37 °C, a marked increase in 2-DOG uptake after exercise was observed in the soleus (P < 0.05) in the absence (0 nM) and presence of insulin (0.2–4 nM) (P < 0.05). A similar postexercise increase in 2-DOG uptake occurred in EDL. Despite the marked increase in glucose uptake and metabolism, no changes in insulin binding were apparent in either EDL or soleus at 37 °C or 18 °C. This study shows that the postexercise increase of glucose disposal does not appear to be directly attributable to increments in insulin binding to slow-twitch and fast-twitch muscles. Also, after exercise the increments in glucose metabolism differ markedly in the two types of muscle.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Pharmacology,General Medicine,Physiology
Cited by
75 articles.
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