Long-term high-fat-diet feeding induces skeletal muscle mitochondrial biogenesis in rats in a sex-dependent and muscle-type specific manner.

Long-term high-fat-diet feeding induces skeletal muscle mitochondrial biogenesis in rats in a sex-dependent and muscle-type specific manner.
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DOI:
10.1186/1743-7075-9-15
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发表时间:
2012-02-21
影响因子:
4.5
通讯作者:
Proenza AM
Proenza AM
中科院分区:
医学3区
文献类型:
--
作者:
Gómez-Pérez Y;Capllonch-Amer G;Gianotti M;Lladó I;Proenza AM

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线粒体功能障碍被认为在胰岛素抵抗的病因学中起着至关重要的作用,其中骨骼肌是主要的组织贡献者。骨骼肌胰岛素和抗氧化剂对高脂饮食(HFD)喂养的反应存在性别差异。本研究的目的是阐明是否有性别二型性的影响HFD喂养骨骼肌线粒体生物合成和脂联素信号通路,以及肌肉类型(氧化或糖酵解)的影响。使用喂食高脂饮食(HFD)或低脂饮食26周的2月龄雄性和雌性Wistar大鼠的腓肠肌和比目鱼肌。线粒体生物发生和氧化损伤标记物,氧化能力和抗氧化防御进行了分析。同时测定血清胰岛素敏感性参数和脂联素信号通路相关蛋白水平。HFD喂养诱导两种性别的线粒体生物合成,但在雄性大鼠中的程度更高。虽然HFD雌性大鼠表现出更大的抗氧化保护,并保持了更好的胰岛素敏感性比他们的男性同行,两种性别表现出受损的反应脂联素,这是更明显的腓肠肌。我们的结论是,HFD大鼠可能会诱导骨骼肌线粒体生物合成,试图补偿脂联素和胰岛素抵抗对氧化代谢的有害后果,HFD喂养的影响是性别依赖性和肌肉类型特异性的。
Mitochondrial dysfunction is thought to play a crucial role in the etiology of insulin resistance, in which skeletal muscle is the main tissue contributor. Sex differences in skeletal muscle insulin and antioxidant responses to high-fat-diet (HFD) feeding have been described. The aim of this study was to elucidate whether there is a sex dimorphism in the effects of HFD feeding on skeletal muscle mitochondrial biogenesis and on the adiponectin signaling pathway, as well as the influence of the muscle type (oxidative or glycolytic). Gastrocnemius and soleus muscles of male and female Wistar rats of 2 months of age fed with a high-fat-diet (HFD) or a low fat diet for 26 weeks were used. Mitochondrial biogenesis and oxidative damage markers, oxidative capacity and antioxidant defences were analyzed. Serum insulin sensitivity parameters and the levels of proteins involved in adiponectin signaling pathway were also determined. HFD feeding induced mitochondrial biogenesis in both sexes, but to a higher degree in male rats. Although HFD female rats showed greater antioxidant protection and maintained a better insulin sensitivity profile than their male counterparts, both sexes showed an impaired response to adiponectin, which was more evident in gastrocnemius muscle. We conclude that HFD rats may induce skeletal muscle mitochondrial biogenesis as an attempt to compensate the deleterious consequences of adiponectin and insulin resistance on oxidative metabolism, and that the effects of HFD feeding are sex-dependent and muscle-type specific.
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