| 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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| 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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