Project/Area Number |
24591218
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | Kanazawa Medical University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KOYA Daisuke 金沢医科大学, 医学部, 教授 (70242980)
|
Co-Investigator(Renkei-kenkyūsha) |
KUME Shinji 滋賀医科大学, 医学部, 特任助教 (00452235)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 糖尿病腎症 / 低たんぱく質食 / オートファジー / mTOR / たんぱく質制限 / ミトコンドリア / 尿細管 / 炎症 / オートファジー / 栄養応答シグナル / サーチュイン / 糖尿病性腎症 / たんぱく質制限食 |
Outline of Final Research Achievements |
In proximal tubule cells of Wistar fatty (fa/fa) rats, type 2 diabetes model, mitochondrial dysfunction such as fragmentation and swelling, oxidative stress and inflammation due to impairment of autophagy by activation of a mammalian target of rapamycin complex1 (mTORC1) exist, resulting in renal injuries including tubule-interstitial fibrosis, tubular cell injuries and apoptosis and decline of renal function. Advanced low-protein diet (including 5% protein) exhibits the tubule cell protective effects through reduction of mTORC1 activation and restoration of autophagy machinery, leading to suppression of progression of renal dysfunction.
|