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首页> 外文期刊>Life sciences >Metformin, but not exercise training, increases insulin responsiveness in skeletal muscle of Sprague-Dawley rats.
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Metformin, but not exercise training, increases insulin responsiveness in skeletal muscle of Sprague-Dawley rats.

机译：二甲双胍可提高Sprague-Dawley大鼠骨骼肌的胰岛素反应性，但不进行运动训练。

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We assessed the effects of combined metformin treatment and exercise training on body composition, on insulin concentration following glucose loading, on insulin-stimulated glucose transport in skeletal muscle, and on muscle glycogen content. Male Sprague-Dawley rats were treated for 35 days with or without metformin (320 mg/kg/day) and/or treadmill exercise training (20 min at 20 m/min, 5 days/wk). Because metformin reduces food intake, pair-fed controls were included. Metformin, training, and pair-feeding all decreased food intake, body weight, and insulin concentration following glucose loading. Metformin and training reduced intra-abdominal fat, but pair feeding did not. In isolated strips derived from soleus, epitrochlearis and extensor carpi ulnaris muscles, metformin increased insulin-stimulated transport of [3H]-2-deoxyglucose by 90%, 89% and 125%, respectively (P < 0.02) and training increased [3H]-2-deoxyglucose transport in the extensor carpi ulnaris muscle only (66%, P < 0.05). Pair-feeding did not alter [3H]-2-deoxyglucose transport. Training increased gastrocnemius muscle glycogen by 100% (P < 0.001). Metformin and pair-feeding did not alter muscle glycogen. We conclude that metformin reverses the maturation-induced impairment of insulin responsiveness in Sprague-Dawley rats by increasing insulin-stimulated glucose transport in skeletal muscle and that this effect is not secondary to reduced food intake. We also conclude that metformin and exercise training may increase insulin sensitivity by different mechanisms, with training causing increased glucose transport only in some muscles and also causing increased muscle glycogen storage.
机译：我们评估了二甲双胍联合治疗和运动训练对身体成分，葡萄糖负荷后胰岛素浓度，骨骼肌中胰岛素刺激的葡萄糖转运以及肌肉糖原含量的影响。雄性Sprague-Dawley大鼠在接受或不接受二甲双胍（320 mg / kg /天）和/或跑步机运动训练（20分钟/分钟，20天/分钟，5天/周）下治疗35天。由于二甲双胍可减少食物摄入，因此纳入了双联对照。葡萄糖负荷后，二甲双胍，训练和成对喂食都会减少食物摄入，体重和胰岛素浓度。二甲双胍和训练减少了腹部脂肪，但配对喂养却没有。在比目鱼肌，上睑肌和尺侧腕腕肌肉分离的条带中，二甲双胍使胰岛素刺激的[3H] -2-脱氧葡萄糖转运分别增加了90％，89％和125％（P <0.02），并且训练增加了[3H] -2-脱氧葡萄糖仅在腕腕腕肌中运输（66％，P <0.05）。配对喂养不会改变[3H] -2-脱氧葡萄糖的转运。训练可使腓肠肌肌肉糖原增加100％（P <0.001）。二甲双胍和成对喂养不会改变肌肉糖原。我们得出的结论是，二甲双胍通过增加骨骼肌中胰岛素刺激的葡萄糖转运来逆转Sprague-Dawley大鼠中成熟的胰岛素反应性损害，并且这种作用并非由于减少食物摄入而引起。我们还得出结论，二甲双胍和运动训练可能通过不同的机制提高胰岛素敏感性，其中训练仅导致某些肌肉的葡萄糖转运增加，还导致肌肉糖原存储增加。

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