Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle
Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle
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DOI：
10.1530/joe-14-0008
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发表时间：
2014-06-01
影响因子：
4
通讯作者：
Garcia-Palmer, Francisco J.
中科院分区：
文献类型：
--
作者：
Capllonch-Amer, Gabriela;Sbert-Roig, Miquel;Garcia-Palmer, Francisco J.
在骨骼肌的线粒体特征中发现了两性异形，雌性大鼠的线粒体质量和功能比雄性大鼠大。脂联素是一种胰岛素增敏脂肪因子，其表达与线粒体功能相关，也在骨骼肌中表达，在骨骼肌中发挥局部代谢作用。本研究的目的是阐明性激素在调节大鼠骨骼肌线粒体功能中的作用及其与脂联素产生的关系。用接受或不接受17 β-雌二醇（E-2）（10 μ mg/kg/48小时，持续4周）的卵巢切除的Wistar大鼠进行体内研究，同时测定用E2（10 nM）、孕酮（Pg; 1 μ M）或睾酮（1 μ M）处理的培养的肌管（L 6 E9）。E-2上调线粒体生物发生和动力学的标志物，以及骨骼肌和L 6 E9中线粒体功能的标志物。虽然在体内补充E-2只部分恢复了卵巢切除术引起的脂联素表达水平下降，这些都增强了E-2和Pg治疗培养的肌管，而睾酮没有表现出任何影响。脂联素受体1的表达增加E-2治疗，在体内和体外，但睾酮降低it. In结论，我们的研究结果是一致的性别二型性先前报道的骨骼肌线粒体功能，并表明E-2是其主要效应，因为它增强线粒体功能，减少氧化应激。此外，我们的数据支持骨骼肌中线粒体功能和脂联素表达之间存在联系的想法，这可能受到性激素的调节。
Sexual dimorphism has been found in mitochondrial features of skeletal muscle, with female rats showing greater mitochondrial mass and function compared with males. Adiponectin is an insulin-sensitizing adipokine whose expression has been related to mitochondrial function and that is also expressed in skeletal muscle, where it exerts local metabolic effects. The aim of this research was to elucidate the role of sex hormones in modulation of mitochondrial function, as well as its relationship with adiponectin production in rat skeletal muscle. An in vivo study with ovariectomized Wistar rats receiving or not receiving 17 beta-estradiol (E-2) (10 mu mg/kg per 48 h for 4 weeks) was carried out, in parallel with an assay of cultured myotubes (L6E9) treated with E2 (10 nM), progesterone (Pg; 1 mu M), or testosterone (1 mu M). E-2 upregulated the markers of mitochondrial biogenesis and dynamics, and also of mitochondrial function in skeletal muscle and L6E9. Although in vivo E-2 supplementation only partially restored the decreased adiponectin expression levels induced by ovariectomy, these were enhanced by E-2 and Pg treatment in cultured myotubes, whereas testosterone showed no effects. Adiponectin receptor 1 expression was increased by E-2 treatment, both in vivo and in vitro, but testosterone decreased it. In conclusion, our results are in agreement with the sexual dimorphism previously reported in skeletal muscle mitochondrial function and indicate E-2 to be its main effector, as it enhances mitochondrial function and diminishes oxidative stress. Moreover, our data support the idea of the existence of a link between mitochondrial function and adiponectin expression in skeletal muscle, which could be modulated by sex hormones.