Molecular mechanisms of the impairment in lipid metabolism
| Project/Area Number |
26460265
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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 |
General anatomy (including histology/embryology)
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脂肪細胞 / ジアシルグリセロールキナーゼ / 中性脂質 / 肥満 / 耐糖能異常 / インスリン抵抗性 / 脂質代謝 / インスリンシグナル / 脂質代謝異常 |
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| Outline of Final Research Achievements |
Present study revealed that mice lacking diacylglycerol kinase epsilon (DGKe) causes abnormal fat deposition and high glucose levels under 40 days of high fat diet (HFD) feeding conditions. Histological examination showed that the size of adipocytes in DGKe-KO mice was greater than those in WT mice. Immunoblot analysis showed the reduced expression of lipolytic enzymes in fat tissue of DGKe-KO mice under HFD conditions. Decreased expression of lipolytic enzymes causes hypertrophy of the adipocytes, leading to obesity. In addition, activation of protein kinase C (PKC) was induced in DGKe-deficient adipocytes. PKC is known to interfere insulin signaling. It suggests that DGKe-KO mice exhibit insulin intolerance via PKC activation.
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Report
(4 results)
Research Products
(18 results)
