| 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)
|
|---|
| 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.
|
