Inhibition of activation of ACCbeta, fatty acids synthase, might be a novel therapeutic strategy against diabetic nephropathy.
Project/Area Number |
25461341
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Metabolomics
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Research Institution | Shiga University of Medical Science |
Principal Investigator |
ISSHIKI KEIJI 滋賀医科大学, 医学部, 非常勤講師 (60378487)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 腎臓病学 / 糖尿病性腎症 / 脂肪毒性 |
Outline of Final Research Achievements |
To investigate the role of ACCβ, fatty acids synthase, in initiation and progression of diabetic nephropathy, we examined the effect of ACCβ using streptozotocin-induced diabetic mouse model in podocyte-specific ACCβ overexpressing mice and proximal tubular cell-specific ACCβ overexpressing mice. Overexpression of ACCβ exacerbated podocyte injury and proximal tubular injury, respectively in streptozotocin-induced diabetic model. Furthermore, in ACCβ overexpressing-cultured podocytes and ACCβ overexpressing-cultured proximal tubular cells, podocyte injury and proximal tubular injury, respectively, were enhanced under high glucose condition. The AMPK activation by AICAR ameliorated both ACCβ-induced podocyte injury and ACCβ-induced proximal tubular injury under high glucose condition. It is suggested that excess of ACCβ contributes to exacerbation of diabetic nephropathy, and the regulation of AMPK/ACCβ pathway may be a new therapeutic strategy to prevent diabetic nephropathy.
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Report
(4 results)
Research Products
(5 results)