2014 Fiscal Year Final Research Report
Investiogation of adiponectin secretion passway
Project/Area Number |
23591353
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Endocrinology
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Research Institution | National Hospital Organization Osaka-Minami Medical Center (2012-2014) Osaka University (2011) |
Principal Investigator |
OHYA Takeshi 独立行政法人国立病院機構(大阪南医療センター臨床研究部), その他部局等, 副室長 (70599315)
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Project Period (FY) |
2011-04-28 – 2015-03-31
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Keywords | アディポサイトカイン / 細胞内小胞輸送 / SNARE蛋白 / 脂肪酸 / 分泌機構 / インスリン抵抗性 / 炎症性反応 |
Outline of Final Research Achievements |
It is still obscure how native anti-inflammatory adipocytokine, adiponectin (APN) secretion can be promoted effectively. The aim of this study is to elucidate the mechanism of APN secretion and to develop a new anti-inflammatory drug for atherosclerosis and diabetes mellitus. The cocktail of seven fatty acids in a physiological ratio could accelerate APN secretion from mouse 3T3-L1 adipocytes. However, even in the same concentration excess of one component of saturated or monounsaturated fatty acid, made it reduced. APN secretion is carried out with intracellular vesicle transport systems, which are governed with membrane-attached proteins called SNARE family including VAMP sub-family. VAMP2 expression was promoted with the fatty acid cocktail load. VAMP3 was suppressed along with saturated fatty acid excess. Inhibition of these molecules made the intracellular APN pool down-sizing. This indicates that they might be candidates for building intracellular APN pools.
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Free Research Field |
内分泌代謝内科
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