| Project/Area Number |
24591159
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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 |
Respiratory organ internal medicine
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| Research Institution | Nagoya City University (2013-2014)
Gifu University (2012) |
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Principal Investigator |
KUNO Toshiya 名古屋市立大学, 医学(系)研究科(研究院), 准教授 (00345779)
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| Co-Investigator(Renkei-kenkyūsha) |
HIROSE Yoshinobu 大阪医科大学, 病理学, 教授 (20293574)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | PPARalpha agonist / lung / neoplasms / obese / hyperlipidemia / hyperinsulinemia / carcinogenesis / PPARα アゴニスト / 肺 / 腫瘍 / 肥満 / 高脂血症 / 高インシュリン血症 / 発がん / PPARαアゴニスト |
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| Outline of Final Research Achievements |
This study was designed to determine whether hypolipidemic agent fenofibrate, PPAR α agonist, can suppress chemically-induced proliferative lesions in the lung of obese hyperlipidemic mice. Male Tsumura Suzuki Obese Diabetic mice were subcutaneously injected with 4-nitroquinoline 1-oxide (4-NQO) to induce lung proliferative lesions, including adenocarcinomas. They were then fed a diet containing fenofibrate for 29 weeks. At week 30, the incidence and multiplicity of pulmonary proliferative lesions were significantly lower in mice treated with 4-NQO and fenofibrate compared with those in mice treated with 4-NQO alone. Fenofibrate significantly reduced the serum insulin and insulin-like growth factor (IGF)-1 levels and decreased the immunohistochemical expression of IGF-1 receptor, p-Akt, and p-Erk1/2 in lung adenocarcinomas. Our results indicate that fenofibrate can prevent the development of 4-NQO-induced proliferative lesions in the lung by modulating the insulin-IGF axis.
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