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Attenuation of insulin resistance by chronic beta(2)-adrenergic agonist treatment - Possible muscle specific contributions

机译：慢性β（2）-肾上腺素能激动剂治疗可减轻胰岛素抵抗-可能的肌肉特异性作用

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A possible mechanism by which chronic clenbuterol treatment causes multiple physiological changes in skeletal muscle that leads to reduced insulin resistance in the obese Zucker rat (fa/fa) was investigated. Animals were gavaged with clenbuterol (CB) (0.8 mgkg(-1).day(-1)), terbutaline (TB) (1.0 mg.kg(-1).day(-1)), or control (CT) vehicle for six weeks. Oral glucose tolerance and insulin responses were markedly improved in CB rats and impaired in TB rats. CB treatment caused a 24-34% gain in muscle mass in all muscle fiber types, and increases in 3-O-methyglucose transport (2-fold) and GLUT4 concentration (57%) in fast twitch glycolytic (FG) muscle. Oxidative capacity was reduced in both FG (47%) and fast twitch oxidative (FO) muscle (30%), but not in slow twitch oxidative (SO) muscle. Null model analysis for receptor occlusion demonstrated that most functional P-adrenoceptors were lost in FO (82%) and FG (89%) fibers, but not in SO fibers. We propose that hypertrophy is the result of continuous direct activation of beta -adrenoceptors while loss in oxidative capacity may be the result of receptor down regulation. Improvements in insulin resistance may have been due, in part, to both increases in lean body mass and specific adaptations in FG muscle. (C) 2001 Elsevier Science Inc. All rights reserved. [References: 40]
机译：研究了慢性克伦特罗治疗引起肥胖的祖克大鼠（fa / fa）引起骨骼肌多种生理变化从而导致胰岛素抵抗降低的可能机制。用克伦特罗（CB）（0.8 mgkg（-1）.day（-1）），特布他林（TB）（1.0 mg.kg（-1）.day（-1））或对照（CT）媒介对动物进行食管六个星期。口服葡萄糖耐量和胰岛素反应在CB大鼠中明显改善，在TB大鼠中受损。 CB治疗使所有肌纤维类型的肌肉质量增加24-34％，并在快速抽搐糖酵解（FG）肌肉中增加3-O-甲基葡萄糖转运（2-倍）和GLUT4浓度（57％）。 FG（47％）和快速抽动氧化（FO）肌肉（30％）的氧化能力均降低，但慢速抽动氧化（SO）肌肉没有降低。受体闭塞的无效模型分析表明，大多数功能性P-肾上腺素能受体在FO（82％）和FG（89％）纤维中丢失，而在SO纤维中丢失。我们认为肥大是β-肾上腺素能受体持续直接激活的结果，而氧化能力的丧失可能是受体下调的结果。胰岛素抵抗的改善可能部分归因于瘦体重的增加和FG肌肉的特殊适应性。 （C）2001 Elsevier Science Inc.保留所有权利。 [参考：40]

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