| Project/Area Number |
15K14989
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Environmental and hygienic pharmacy
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| Research Institution | Gifu Pharmaceutical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中西 剛 岐阜薬科大学, 薬学部, 准教授 (50303988)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | リポカリン / 尿中排泄蛋白質 / メタボリック症候群 / アンドロゲン / トランスジェニックマウス |
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| Outline of Final Research Achievements |
In order to investigate the metabolic roles of MUP1 in obesity development, we generated the transgenic mice that overexpress MUP1 under the control of CAG promoter (MUP1-TG mice). Expression of MUP1 was very high in various tissues, including adipose tissue, of MUP1-TG mice compared to those of wild-type mice. Overexpression of MUP1 protected short-term high-fat diet (HFD)-induced lipidemia and body weight gain with increasing adipose tissue mass. In vitro model of adipocyte differentiation using mouse embryonic fibroblasts, overexpression of MUP1 suppressed the mRNA levels of adipocyte-related genes in the early stage, and prevent lipid droplet accumulation. Furthermore, the protection of HFD-induced lipidemia and body weight gain in MUP1-TG mice was attenuated by heterozygous peroxisome proliferator-activated receptor γ knockouts. Our findings suggest a novel role of MUP1 which may maintain metabolic homeostasis by regulation of adipocyte differentiation in the early stage.
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