| Project/Area Number |
23390243
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Kumamoto University |
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Principal Investigator |
ARAKI Eiichi 熊本大学, 生命科学研究部, 教授 (10253733)
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| Co-Investigator(Kenkyū-buntansha) |
KONDO Tatsuya 熊本大学, 大学院・生命科学研究部, 助教 (70398204)
|
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| Project Period (FY) |
2011-11-18 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥9,750,000 (Direct Cost: ¥7,500,000、Indirect Cost: ¥2,250,000)
Fiscal Year 2013: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
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| Keywords | 糖尿病 / 小胞体ストレス / 分子シャペロン / BiP / HSP72 |
|---|
| Research Abstract |
Induction of molecular chaperone, such as BiP or HSP72 on insulin sensitive tissues improved glucose homeostasis, insulin signaling and ER stress resistance both in vitro and in vivo. On the other hand, attenuation of BiP or HSP72 resulted in impairment of glucose handling and less ER stress resistance.
On analyses of gene expressions when HSP72 was over expressed, AMPK, PGC-1a and Sirt1 mRNA were un-regulated. These molecules may exert anti-diabetic effects upon HSP72 induction.
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