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1 Department of Sports Sciences, University of Toyko, College of Arts and Sciences, Meguro-ku, Komaba, Tokyo, Japan
2 Department of Kinesiology, University of Waterloo, waterloo, Ontario, Canada
* To whom correspondence should be addressed. E-mail: cc27704{at}mail.ecc.u-tokyo.ac.jp.
We compared the changes in MCT1 and MCT4 proteins in heart and skeletal muscles in sedentary control and streptozotocin (STZ)-induced diabetic rats (3 weeks), and in trained (3 weeks) control and STZ-induced diabetic animals. In non-diabetic animals, training increased MCT1 in plantaris (+51%, P<0.01), but not in soleus (+9%) or the heart (+14%). MCT4 was increased in the plantaris (+48%, P<0.01), but not in the soleus muscles of trained, non-diabetic animals. In sedentary diabetic animals MCT1 was reduced in heart (-30%), and in the plantaris (-31%, P<0.01) and soleus (-26%) muscles. MCT4 content was also reduced in sedentary, diabetic animals in the plantaris (-52%, P<0.01) and soleus (-25%) muscles. In contrast, in trained diabetic animals MCT1 and MCT4 in heart and/or muscle were similar to those of sedentary, non-diabetic animals (P>0.05), but were markedly greater than in the sedentary diabetic animals (MCT1: plantaris +63%, soleus +51%, heart +51% (P>0.05); MCT4: plantaris +107%, soleus +17% (P>0.05)). These studies have shown that a) with STZ-induced diabetes MCT1 and MCT4 are reduced in skeletal muscle and/or heart, and b) that exercise training alleviated these diabetes-induced reductions.
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