| Project/Area Number |
22590971
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | University of Toyama |
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Principal Investigator |
USUI Isao 富山大学, 大学病院, 講師 (50377272)
|
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| Co-Investigator(Kenkyū-buntansha) |
TOBE Kazuyuki 富山大学, 大学院・医学薬学研究部(医学), 教授 (30251242)
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| Co-Investigator(Renkei-kenkyūsha) |
MINOKOSHI Yasuhiko 生理学研究所, 発達生理学研究系, 教授 (10200099)
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| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2012: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Keywords | 内科系臨床医学 / 代謝学 / 脂肪組織 / マクロファージ / メタボリックシンドローム / インターロイキン10 |
|---|
| Research Abstract |
In this study, we investigated the relationship between adipose tissue M1/M2 macrophages and insulin sensitivity, focusing on the roles of M2 macrophage and interleukin10 （IL-10). Telmisartan, an angiotensin II type I receptor blocker, induced M2 polarity of adipose tissue macrophages with its PPARγ-stimulating activity, while adipose tissue hypoxia induced the M1 polarity. M2 macrophage ablation mice, in which the number of M2 macrophage could be decreased by adding diphtheria toxin, showed smaller adipocyte size and improved insulin sensitivity. The activation of IL-10 signaling in hypothalamus increased the expression of mitochondria-related genes in skeletal muscle and improved inulin sensitivity.
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