Reveal for the role of intracellular control of sodium ion and mechanism of mitochondrial fission and fusion on renal tubular disorder

2014 Fiscal Year Final Research Report

• Project/Area Number: 25870281
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Chemical biology; Metabolomics
• Research Institution: University of Yamanashi
• Principal Investigator: SAITOH Sei 山梨大学, 総合研究部, 助教 (10456444)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 糖尿病性尿細管障害 / SBF-SEM / ミトコンドリア / ヒト尿細管培養細胞 / フロリジン / SGLT阻害剤 / オートファジー / SGLT2

Outline of Final Research Achievements

The C57BL6J mice were divided two groups fed with standard (STD) and high fat diet (HFD). The mouse body weights and blood glucose levels of HFD group were significantly higher than STD group’s at 20 weeks of age. And after administration of phlorizine (adPLZ) of HFD group, the blood glucose levels were significantly decreased than before. The proximal tubule segment1 were 3 demential analyzed with serial block face-scanning electron microscope (SBF-SEM). In STD group, the numerous lysosome (Ly) apical on the huge size of mitochondria(Mit) were confirmed in the epithelium of the proximal tubule segment 1. The giant autophagosome (At) and, small fragmented Mit were in HFD group. After adPLZ of HFD group, the giant At were decreased, but small and medium size of Ly were increased, and secondly the branched Mit were found. On high glucose culture condition (D-glucose 400mg/dl) the fragmented Mit were re-branched after adPLZ of human primary culture of proximal tubular epithelial cells.

Free Research Field

人体解剖学