Dysfunction of Mitochondrial Dynamics in Drosophila Model of Diabetic Nephropathy

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 Drosophila 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 Drosophila. High-sucrose diet induced mitochondria fusion in nephrocytes by increasing Opa1 and Marf expression. These findings establish Drosophila 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.

Automated summary

In this study, a Drosophila model of diabetic nephropathy was established by feeding flies a chronic high-sucrose diet, which led to reduced lifespan, increased lipid droplets, and morphological abnormalities in nephrocytes. The high-sucrose diet also induced mitochondrial fusion in nephrocytes. These findings suggest that Drosophila can serve as a valuable model for studying the pathogenesis and treatment of DN.