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首页> 外文期刊>Biochimica et biophysica acta. Bioenergetics >Alterations in the mitochondrial regulatory pathways constituted by the nuclear co-factors PGC-1alpha or PGC-1beta and mitofusin 2 in skeletal muscle in type 2 diabetes.
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Alterations in the mitochondrial regulatory pathways constituted by the nuclear co-factors PGC-1alpha or PGC-1beta and mitofusin 2 in skeletal muscle in type 2 diabetes.

机译：在2型糖尿病中核心肌肉骨骼肌肉中的核心共同因子PGC-1α或PGC-1β和MITOFUSIN 2构成的线粒体调节途径的改变。

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Muscle mitochondrial metabolism is regulated by a number of factors, many of which are responsible for the transcription of nuclear genes encoding mitochondrial proteins such as PPARdelta, PGC-1alpha or PGC-1beta. Recent evidence indicates that proteins participating in mitochondrial dynamics also regulate mitochondrial metabolism. Thus, in cultured cells the mitochondrial fusion protein mitofusin 2 (Mfn2) stimulates respiration, substrate oxidation and the expression of subunits involved in respiratory complexes. Mitochondrial dysfunction has been reported in skeletal muscle of type 2 diabetic patients. Reduced mitochondrial mass and defective activity has been proposed to explain this dysfunction. Alterations in mitochondrial metabolism may be crucial to account for some of the pathophysiological traits that characterize type 2 diabetes. Skeletal muscle of type 2 diabetic patients shows reduced expression of PGC-1alpha, PGC-1beta, and Mfn2. In addition, a differential response to bilio-pancreatic diversion-induced weight loss in non-diabetic and type 2 diabetic patients has been reported. While non-diabetic morbidly obese subjects showed an increased expression of genes encoding Mfn2, PGC-1alpha, PGC-1beta, PPARdelta or SIRT1 in response to bariatric surgery-induced weight loss, no effect was detected in type 2 diabetic patients. These observations suggest the existence of a heritable component responsible for the abnormal control of the expression of genes encoding for modulators of mitochondrial biogenesis/metabolism, and which may participate in the development of the disease.
机译：肌肉线粒体代谢由许多因素进行调节，其中许多因素负责编码线粒体蛋白如pPARTELTA，PGC-1α或PGC-1Beta的核基因的转录。最近的证据表明，参与线粒体动力学的蛋白质也调节线粒体代谢。因此，在培养的细胞中，线粒体融合蛋白Mitofusin 2（MFN2）刺激呼吸，底物氧化和呼吸复合物中所涉及的亚基的表达。在2型糖尿病患者的骨骼肌中报道了线粒体功能障碍。已经提出了减少的线粒体质量和有缺陷的活性来解释这种功能障碍。线粒体代谢的改变可能是至关重要的，以考虑表征2型糖尿病的病理生理学特征。 2型糖尿病患者的骨骼肌显示出PGC-1α，PGC-1Beta和MFN2的表达减少。此外，还报道了对非糖尿病和2型糖尿病患者的抗纤维胰腺引起的体重减轻的差异反应。虽然非糖尿病病态肥胖受试者表现出编码MFN2，PGC-1α，PGC-1Beta，PPARTELTA或SIRT1的基因表达增加，但响应于慢性手术诱导的体重减轻，但在2型糖尿病患者中没有检测到任何效果。这些观察结果表明，存在遗传成分，其负责对编码线粒体生物发生/代谢的调节剂表达的异常控制，并且可能参与疾病的发展。

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