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首页> 外文期刊>Zoological Science >Long term adrenal insufficiency induces skeletal muscle atrophy and increases the serum levels of active form myostatin in rat serum
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Long term adrenal insufficiency induces skeletal muscle atrophy and increases the serum levels of active form myostatin in rat serum

机译：长期肾上腺皮质功能不全会诱发骨骼肌萎缩并增加大鼠血清中肌肉生长抑制素的活性水平

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Skeletal muscle wasting is a common symptom in the adrenal insufficiency such as Addison's disease. Although it has been suspected that several cytokines and/or growth factors are responsible for the manifestation of the symptom, the precise mechanisms underlying the phenomenon have so far been poorly understood. Myostatin is predominantly expressed in skeletal muscles and involved in the regulation of skeletal muscle mass. Recently, several reports indicated that myostatin is secreted into the circulation and the increased levels of circulating myostatin is associated with the induction of skeletal muscle wasting in adult animals. We, therefore, hypothesized that the increased levels of circulating myostatin may account for the development of skeletal muscle wasting in adrenal insufficiency. To test the validity of this hypothesis, we compared the serum levels of myostatin in normal with those in bilaterally adrenalectomized (ADX) rats, a model of Addison's disease, by Western blot analysis. The active form of myostatin (13 kDa) was barely detectable in the sera collected either 1 month or 2 month after adrenalectomy, but present at conspicuously detectable levels in those obtained 3 month after the operation, while the total amounts of myostatin proteins (sum of the precursor and the active forms) remained constant at all the time points examined post-operatively. These results are consistent with the hypothesis that the increased serum levels of active form of myostatin protein, induced yet unknown post-translational control mechanisms may be responsible, at least in part, for the muscle wasting associated with the adrenal insufficiency syndromes.
机译：骨骼肌萎缩是肾上腺功能不全的常见症状，例如艾迪生氏病。尽管已经怀疑几种细胞因子和/或生长因子与症状的表现有关，但迄今为止，对该现象的确切机制尚不甚了解。肌生长抑制素主要在骨骼肌中表达，并参与骨骼肌质量的调节。最近，一些报道表明肌生长抑制素被分泌到循环系统中，循环肌生长抑制素水平的升高与成年动物骨骼肌消耗的减少有关。因此，我们假设循环肌生长抑制素水平的升高可能是肾上腺功能不全导致骨骼肌萎缩的原因。为了验证该假设的有效性，我们通过Western印迹分析比较了正常人和双侧肾上腺切除术（ADX）大鼠（一种Addison病模型）的血清肌肉生长抑制素水平。在肾上腺切除术后1个月或2个月收集的血清中几乎无法检测到肌生长抑制素的活性形式（13 kDa），但在术后3个月获得的血清中却以明显可检测的水平存在，而肌生长抑制素蛋白的总量（在手术后检查的所有时间点，前体和活性形式均保持恒定。这些结果与这样的假设相一致，即，血清肌抑制素蛋白活性形式的血清水平升高，诱导的翻译后控制机制尚不清楚，这可能至少部分是与肾上腺功能不全综合征相关的肌肉消瘦的原因。

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