Decreased monocarboxylate transporter 1 in rat soleus and EDL muscles exposed to clenbuterol

被引:19
|
作者
Kitaura, T [1 ]
Tsunekawa, N
Hatta, H
机构
[1] Kanazawa Univ, Fac Pharmaceut Sci, Kanazawa, Ishikawa 9201192, Japan
[2] Univ Tokyo, Dept Life Sci, Tokyo 1538902, Japan
关键词
lactate dehydrogenase; myosin heavy chain; beta; 2-agonist; transition;
D O I
10.1152/jappl.2001.91.1.85
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
We hypothesized that a shift in muscle fiber type induced by clenbuterol would change monocarboxylate transporter 1 (MCT1) content and activity of lactate dehydrogenase (LDH) and isoform pattern and shift myosin heavy chain (MHC) pattern in soleus (Sol) and extensor digitorum longus (EDL) of male rats. In the clenbuterol-administered rats (2.0 mg.kg(-1).day(-1) subcutaneously for 4 wk), the ratio of muscle weight to body weight increased in the Sol (P < 0.05) and the EDL (P < 0.01). Clenbuterol induced the appearance of fast MHC2D and decreased slow MHC1 in Sol (13%) but had no effect on EDL. The MHC pattern of Sol changed from slow to fast type. Clenbuterol increased LDH-specific activity (P, 0.01) and the ratio of the muscle-type isozyme of LDH to the heart type (P, 0.05) in Sol. The LDH total activity of the EDL muscle was also increased (P, 0.05). Furthermore, MCT1 content significantly (P, 0.05) decreased in both Sol and EDL (27 and 52%, respectively). This study suggests that clenbuterol might mediate the shift of MHC from slow to fast type and the changes in the regulation of lactate metabolism. Novel to this study is the observation that clenbuterol decreases MCT1 content in the hindlimb muscles and that the decrease in MCT1 is not muscle-type specific. It may suggest that the genetic expressions of individual factors involving slow-type MHC, heart-type isozyme of LDH, and MCT1 are associated with one another but are regulated independently.
引用
收藏
页码:85 / 90
页数:6
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