The role of Sirtuin on diabetic nephropatfunctionhy based on maintaining mitochondrial

2016 Fiscal Year Final Research Report

• Project/Area Number: 26860651
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Kidney internal medicine
• Research Institution: Kanazawa Medical University
• Principal Investigator: WATANABE Ai (竹田愛) 金沢医科大学, 医学部, 助教 (70625722)
• Research Collaborator: KITADA Munehiro 金沢医科大学, 医学部, 准教授 (40434469) ; KOYA Daisuke 金沢医科大学, 医学部, 教授 (70242980)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 糖尿病腎症 / Sirt3 / ミトコンドリア / 酸化ストレス

Outline of Final Research Achievements

Mitochondrial (Mt) oxidative stress, which is important for the pathogenesis of diabetic nephropathy, is caused by the breakdown of active oxygen species production / antioxidant balance and Mt function decline / homeostatic maintenance. The NAD + dependent deacetylase (Sirt 3) plays an important role in controlling Mt redox and Mt homeostasis. In renal proximal tubular cells of Zucker Diabetic fatty rats, the increase in NAD + consumption posibly due to the increased expression of CD38, which is known as NAD+ degrading enzyme, and the decrease in Sirt 3 function contributed to the enhancement of Mt oxidative stress。And than, the autophagy function is impaired in the kidney of diabetic rats, resulting in the accumulation of abnormal Mt and the breakdown of Mt homeostasis, which is involved in the initiation and progression of diabetic nephropathy.

Free Research Field

糖尿病