| Project/Area Number |
19591065
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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 |
|---|
Principal Investigator |
ISHIDA Hitoshi Kyorin University, 医学部, 教授 (80212893)
|
|---|
| 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)
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|---|
| Project Period (FY) |
2007 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 2型糖尿病 / インスリン分泌 / 酸化ストレス / マクロファージ / 膵β細胞 / 脂肪細胞 / MCP-1 |
|---|
| Research Abstract |
The increased release of MCP-1 was observed from pancreatic MIN6 β cells under diabetic conditions, leading to the enhancement of macrophage infiltration into pancreatic islets. And increased endogenous oxidative stress in β cells could be related to its underlying mechanism. In addition, the release of MCP-1 and VEGF was also found to be increased from 3T3L1 adipocytes. The enhancement of endogenous oxidative stress was similarly speculated to be the pathogenic mechanism of their increased secretion, and in terms of released MCP-1, we deduce that the IkB- dependent pathway is, at lease in part, important as a common distal signaling in both pancreatic β cells and adipocytes.
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