Mitochondrial dysregulation in the pathogenesis of diabetes: potential for mitochondrial biogenesis-mediated interventions.

Experimental Diabetes Research Pub Date : 2012-01-01 Epub Date: 2011-12-01 DOI:10.1155/2012/642038
Anna-Maria Joseph, Denis R Joanisse, Richard G Baillot, David A Hood
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引用次数: 113

Abstract

Muscle mitochondrial metabolism is a tightly controlled process that involves the coordination of signaling pathways and factors from both the nuclear and mitochondrial genomes. Perhaps the most important pathway regulating metabolism in muscle is mitochondrial biogenesis. In response to physiological stimuli such as exercise, retrograde signaling pathways are activated that allow crosstalk between the nucleus and mitochondria, upregulating hundreds of genes and leading to higher mitochondrial content and increased oxidation of substrates. With type 2 diabetes, these processes can become dysregulated and the ability of the cell to respond to nutrient and energy fluctuations is diminished. This, coupled with reduced mitochondrial content and altered mitochondrial morphology, has been directly linked to the pathogenesis of this disease. In this paper, we will discuss our current understanding of mitochondrial dysregulation in skeletal muscle as it relates to type 2 diabetes, placing particular emphasis on the pathways of mitochondrial biogenesis and mitochondrial dynamics, and the therapeutic value of exercise and other interventions.

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糖尿病发病机制中的线粒体失调:线粒体生物发生介导干预的潜力。
肌肉线粒体代谢是一个受到严格控制的过程,涉及核基因组和线粒体基因组的信号通路和因子的协调。也许调节肌肉代谢最重要的途径是线粒体生物发生。作为对运动等生理刺激的反应,逆行信号通路被激活,允许细胞核和线粒体之间的串扰,上调数百个基因,导致线粒体含量增加和底物氧化增加。患有2型糖尿病,这些过程可能变得失调,细胞对营养和能量波动的反应能力减弱。这一点,再加上线粒体含量减少和线粒体形态改变,与这种疾病的发病机制直接相关。在本文中,我们将讨论我们目前对骨骼肌线粒体失调的理解,因为它与2型糖尿病有关,特别强调线粒体生物发生和线粒体动力学的途径,以及运动和其他干预措施的治疗价值。
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来源期刊
Experimental Diabetes Research
Experimental Diabetes Research 医学-内分泌学与代谢
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3-8 weeks
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