| Project/Area Number |
25462160
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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 |
Cardiovascular surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOMORI KIMIHIRO 名古屋大学, 大学院医学系研究科, 教授 (40225587)
BANNO HIROSHI 名古屋大学, 医学部附属病院, 講師 (80584721)
KODAMA AKIO 名古屋大学, 医学部附属病院, 講師 (10528748)
MAEKAWA TAKASHI 名古屋大学, 医学部附属病院, 病院助教 (70732684)
SHIBATA REI 名古屋大学, 大学院医学系研究科, 寄附講座准教授 (70343689)
SUGIMOTO MASAYUKI 名古屋大学, 医学部附属病院, 病院助教 (00447814)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 動脈瘤、アディポネクチン / 大動脈瘤 / アディポネクチン / PPAR-ガンマ agonist / アディポサイトカイン |
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| Outline of Final Research Achievements |
Abdominal aortic aneurysm (AAA) is a feature of various vascular disorders including atherosclerosis and hypertension. A peroxisome proliferator-activated receptor-γ(PPARγ) ligand, pioglitazone is a relative new class of oral agent for the treatment of type 2 diabetes and insulin resistance. Pioglitazone has beneficial effects on endothelial function, hypertension and atherosclerosis. Here we investigated the effect of pioglitazone on AAA. The AAA model was induced by CaCl2 in male mice, and mice were treated with pioglitazone as food admixture at a concentration of 0.01%. Treatment of wild-type (WT) mice with pioglitazone attenuated CaCl2-induced aneurysm formation in mice. Pioglitazone also increased plasma adiponectin level in WT mice. However, adiponectin-deficient mice did not affect in CaCl2-induced aneurysm formation. These data provide direct evidence that pioglitazone protects against CaCl2-induced aneurysm formation via an adiponectin-independent mechanism.
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