Kim Kiyoung, Cha Sun Joo, Choi Hyun-Jun, Kang Jeong Suk, Lee Eun Young
Department of Medical Biotechnology, Soonchunhyang University, Asan 31538, Korea.
Department of Medical Sciences, Soonchunhyang University, Asan 31538, Korea.
Life (Basel). 2021 Jan 18;11(1):67. doi: 10.3390/life11010067.
Although mitochondrial dysfunction is associated with the development and progression of diabetic nephropathy (DN), its mechanisms are poorly understood, and it remains debatable whether mitochondrial morphological change is a cause of DN. In this study, a DN model was established by treating a chronic high-sucrose diet that exhibits similar phenotypes in animals. Results showed that flies fed a chronic high-sucrose diet exhibited a reduction in lifespan, as well as increased lipid droplets in fat body tissue. Furthermore, the chronic high-sucrose diet effectively induced the morphological abnormalities of nephrocytes in . High-sucrose diet induced mitochondria fusion in nephrocytes by increasing Opa1 and Marf expression. These findings establish as a useful model for studying novel regulators and molecular mechanisms for imbalanced mitochondrial dynamics in the pathogenesis of DN. Furthermore, understanding the pathology of mitochondrial dysfunction regarding morphological changes in DN would facilitate the development of novel therapeutics.
尽管线粒体功能障碍与糖尿病肾病（DN）的发生和发展相关，但其机制仍知之甚少，线粒体形态变化是否为DN的病因仍存在争议。在本研究中，通过给动物喂食慢性高糖饮食建立了DN模型，该模型在动物中表现出相似的表型。结果显示，喂食慢性高糖饮食的果蝇寿命缩短，脂肪体组织中的脂滴增加。此外，慢性高糖饮食有效地诱导了肾细胞的形态异常。高糖饮食通过增加Opa1和Marf的表达诱导肾细胞中的线粒体融合。这些发现确立了该模型作为研究DN发病机制中线粒体动力学失衡的新型调节因子和分子机制的有用模型。此外，了解DN中线粒体功能障碍与形态变化相关的病理学将有助于新型疗法的开发。
