首页> 美国卫生研究院文献>Physiological Reports >Net protein balance correlates with expression of autophagy mitochondrial biogenesis and fat metabolism‐related genes in skeletal muscle from older adults
【2h】

Net protein balance correlates with expression of autophagy mitochondrial biogenesis and fat metabolism‐related genes in skeletal muscle from older adults

机译:净蛋白平衡与老年人骨骼肌中的自噬线粒体生物发生和脂肪代谢相关基因的表达相关

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

The mechanisms leading to sarcopenia, the main cause for frailty in older adults, are still unclear. Autophagy and the ubiquitin‐proteasome system (UPS) may play a role in mediating muscle protein breakdown related to sarcopenia. In addition to loss of muscle mass, compromised muscle performance observed in sarcopenic patients has been linked to muscle mitochondria dysfunction. Increased fat deposition and fat cell infiltration in muscle frequently seen in skeletal muscle of older adults may play an additional role for the pathogenesis of sarcopenia. Therefore, the first objective of this study was to understand differences in expression of genes related to autophagy, UPS, mitochondrial biogenesis, and fat metabolism in skeletal muscle of older adults compared with young adults. Our second objective was to determine the correlation between whole body protein kinetics (WBPK) and gene expression with age. Real‐time quantitative PCR was used to determine the relative expression of targeted genes, and hierarchical regression analysis was used to determine if age had a moderating effect on the correlation between expression of targeted genes and WBPK. Increases in the expression of autophagy‐related genes and fat metabolism‐related genes were observed in muscle of older adults compared with young adults. In addition, age enhanced the negative correlations between mitochondrial biogenesis genes and net protein balance. These results suggest that dysregulated gene expression of mitochondrial biogenesis could play a role in muscle loss in older adults.
机译:导致康迟腺尼亚的机制,老年人体现的主要原因,尚不清楚。自噬和泛素 - 蛋白酶体系(UPS)可能在介导与SARCOPENIA相关的肌肉蛋白分解中发挥作用。除了肌肉质量损失外,患有肌肉发血患者中观察到的损伤肌肉表现与肌肉线粒体功能障碍有关。在老年人的骨骼肌中经常看到的肌肉中经常看到的脂肪沉积和脂肪细胞浸润可能在肌肉发病机制中发挥额外作用。因此,本研究的第一个目的是了解与年轻成年人相比,在老年人的骨骼肌中表达与自噬,UPS,线粒体生物发生和脂肪代谢相关的基因表达的差异。我们的第二个目的是确定全身蛋白质动力学(WBPK)与年龄的基因表达之间的相关性。使用实时定量PCR来确定靶向基因的相对表达,并且使用分层回归分析来确定年龄是否对靶向基因和WBPK表达之间的相关性进行调节效果。与年轻成人相比,在老年人的肌肉中观察到自噬相关基因和脂肪代谢相关基因的表达增加。此外,年龄增强了线粒体生物发生基因和净蛋白质平衡之间的负相关性。这些结果表明,心脏粒细胞生物发生的失调基因表达可能在老年人的肌肉损失中发挥作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号