2014 Fiscal Year Final Research Report
Enhanced PDGF signaling contributes adipose tissue angiogenesis, expansion, and systemic glucose intolerance in obesity.
Project/Area Number |
24591318
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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 |
Metabolomics
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Research Institution | University of Toyama |
Principal Investigator |
WADA Tsutomu 富山大学, 大学院医学薬学研究部 (薬学), 講師 (00419334)
|
Co-Investigator(Kenkyū-buntansha) |
SASAOKA Toshiyasu 富山大学, 医学薬学研究部, 教授 (00272906)
|
Co-Investigator(Renkei-kenkyūsha) |
SASAHARA Masakiyo 富山大学, 医学薬学研究部, 教授 (20154015)
ISHII Yoko 富山大学, 医学薬学研究部, 準教授 (00361949)
|
Research Collaborator |
小野木 康弘
神谷 知江
稲田 健人
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 血管新生 / 脂肪組織肥大化 / 慢性炎症 / エネルギー消費 |
Outline of Final Research Achievements |
Adipose tissues expand with neovessel formations. We found that the angiogenic factor platelet derived growth factor (PDGF) and its receptor (PDGFRb) are highly increased in the adipose tissue when mice were fed on high-fat diet (HFD). In the present study, we examined the impact of PDGF signaling on adipose tissue hypertrophy and metabolic phenotype in obesity by using systemic or central nerve specific PDGFRb knockout mice. We found that PDGF signal was important for adipose tissue angiogenesis in obesity, and the inhibition of angiogenesis augmented energy expenditure and obese-resistant phenotype in mice. As the underlying mechanism, the compensation for insufficient lipid storage in the adipose tissue appears to be involved in the obesity-resistant phenotype, rather than the lack of direct action of PDGF in the hypothalamic neurons.
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Free Research Field |
糖尿病学
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