| Project/Area Number |
25461363
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Kyorin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
INUKAI Koichi 杏林大学, 医学部, 准教授 (20333007)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 2型糖尿病 / マクロファージ / 膵β細胞 / 脂肪細胞 / MCP-1 / 内因性酸化ストレス / Astaxanthin / JNK経路 / ２型糖尿病 / 脂肪脂肪 / VEGF / PI3K依存性経路 |
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| Outline of Final Research Achievements |
We analyzed the influence of antioxidant astaxanthin on monocyte chemoattractant protein-1 (MCP-1), a key factor on free fatty acids-induced chronic inflammation, by using mouse insulinoma (MIN6) cells long-term treated with high concentration of palmitate. While palmitate significantly increased endogenous oxidative stress and enhanced MCP-1 secretion in MIN6 cells, astaxanthin as well as SP600125, a JNK-specific inhibitor, clearly reduced this enhanced MCP-1. Furthermore, astaxanthin attenuated JNK phosphorylation, and also diminished endoplasmic reticulum stress enhanced by palmitate.
Taken together, astaxanthin can suppress MCP-1 release, which is up-regulated by palmitate, through the inactivity of JNK pathways on MIN6 cells. The results of this study raise the possibility that astaxanthin would become a new preventive tool for the progression of β cell dysfunction observed in type 2 diabetes with clinical dyslipidemia.
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