| Project/Area Number |
22590993
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
|
|---|
| Research Institution | Kyorin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAGAMATSU Shinya 杏林大学, 医学部, 教授 (80231489)
YOSHIMOTO Katsuhiko 杏林大学, 医学部, 講師 (20271257)
INUKAI Kouichi 杏林大学, 医学部, 准教授 (20333007)
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| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 2型糖尿病 / 膵ラ氏島 / マクロファージ / サイトカイン / 熱ショック蛋白 / 膵β細胞 / 脂肪細胞 / インスリン分泌 / MCP-1 / VEGF / 酸化ストレス / アンカップリング |
|---|
| Research Abstract |
The JNK and IκB- dependent pathways were deduced, at least in part, as common mechanisms for the increased release of MCP-1 from pancreatic MIN6βcells and 3T3L1 adipocytes under diabetic conditions, leading to the enhancement of macrophage infiltration into pancreatic islets and adipose tissues, respectively. In addition, we explored the cytoprotective mechanism to reduce MCP-1 release from 3T3L1 adipocytes, and it was found that the induction of metabolic uncoupling in mitochondria to activate the AMP-activated protein kinase and also of heat shock protein 72 at 41℃could be important in these cells for the reduction of MCP-1 release.
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