2014 Fiscal Year Final Research Report
Elucidation of mechanism by which low protein diet suppresses progression of diabetic nephropathy through activation of autophagy in tubular cells
| Project/Area Number |
24591218
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOYA Daisuke 金沢医科大学, 医学部, 教授 (70242980)
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| Co-Investigator(Renkei-kenkyūsha) |
KUME Shinji 滋賀医科大学, 医学部, 特任助教 (00452235)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 糖尿病腎症 / 低たんぱく質食 / オートファジー / mTOR |
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| 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.
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| Free Research Field |
糖尿病 腎臓病
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