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肥胖 Zucker 大鼠肌肉中的卫星细胞增殖减少,但通过负荷可恢复。

Satellite cell proliferation is reduced in muscles of obese Zucker rats but restored with loading.

作者信息

Peterson Jonathan M, Bryner Randall W, Alway Stephen E

机构信息

Laboratory of Muscle Biology and Sarcopenia, Division of Exercise Physiology, West Virginia School of Medicine, Robert C. Byrd Health Science Center, West Virginia Univ., Morgantown, WV 26506-9227, USA.

出版信息

Am J Physiol Cell Physiol. 2008 Aug;295(2):C521-8. doi: 10.1152/ajpcell.00073.2008. Epub 2008 May 28.

Abstract

The obese Zucker rat (OZR) is a model of metabolic syndrome, which has lower skeletal muscle size than the lean Zucker rat (LZR). Because satellite cells are essential for postnatal muscle growth, this study was designed to determine whether reduced satellite cell proliferation contributes to reduced skeletal mass in OZR vs. LZR. Satellite cell proliferation was determined by a constant-release 5-bromo-2-deoxyuridine (BrdU) pellet that was placed subcutaneously in each animal. Satellite cell proliferation, as determined by BrdU incorporation, was significantly attenuated in control soleus and plantaris muscles of the OZR compared with that shown in the LZR. To determine whether this attenuation of satellite cell activity could be rescued in OZR muscles, soleus and gastrocnemius muscles were denervated, placing a compensatory load on the plantaris muscle. In the LZR and the OZR after 21 days of loading, increases of approximately 25% and approximately 30%, respectively, were shown in plantaris muscle wet weight compared with that shown in the contralateral control muscle. The number of BrdU-positive nuclei increased similarly in loaded plantaris muscles from LZR and OZR. Myogenin, MyoD, and Akt protein expressions were lower in control muscles of OZR than in those of the LZR, but they were all elevated to similar levels in the loaded plantaris muscles of OZR and LZR. These data indicate that metabolic syndrome may reduce satellite cell proliferation, and this may be a factor that contributes to the reduced mass in control muscles of OZR; however, satellite cell proliferation can be restored with compensatory loading in OZR.

摘要

肥胖型 Zucker 大鼠(OZR)是代谢综合征的一种模型,其骨骼肌大小比瘦型 Zucker 大鼠(LZR)小。由于卫星细胞对出生后肌肉生长至关重要,本研究旨在确定卫星细胞增殖减少是否导致 OZR 与 LZR 相比骨骼肌质量降低。通过将持续释放的 5-溴-2-脱氧尿苷(BrdU)微丸皮下植入每只动物来测定卫星细胞增殖。与 LZR 相比,OZR 的对照比目鱼肌和跖肌中,通过 BrdU 掺入测定的卫星细胞增殖明显减弱。为了确定 OZR 肌肉中这种卫星细胞活性的减弱是否可以恢复,对其比目鱼肌和腓肠肌进行去神经支配,给跖肌施加代偿性负荷。在加载 21 天后,与对侧对照肌肉相比,LZR 和 OZR 的跖肌湿重分别增加了约 25%和约 30%。来自 LZR 和 OZR 的加载跖肌中 BrdU 阳性核的数量同样增加。OZR 对照肌肉中的生肌调节因子、肌分化抗原和蛋白激酶 B 蛋白表达低于 LZR,但在 OZR 和 LZR 的加载跖肌中它们均升高到相似水平。这些数据表明,代谢综合征可能会降低卫星细胞增殖,这可能是导致 OZR 对照肌肉质量降低的一个因素;然而,通过 OZR 中的代偿性负荷可以恢复卫星细胞增殖。

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