| Project/Area Number |
24890027
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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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) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 血糖値 / インスリン抵抗性 / ジアシルグリセロールキナーゼ / 高脂肪食 / 血糖調節機構 / DGK / 糖脂質代謝 / GLUT / PPAR |
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| Research Abstract |
Diacylglycerol kinase epsilon knock out (DGKe-KO) mouse was fed with high fat diet (HFD) for 40 days. This induced acute increase in body weight and white adipose tissue mass, and led to severe lipid accumulation in the liver. Since hepatic lipid accumulation is known as a symptom of insulin resistance, we performed glucose tolerance test. It revealed that HFD fed DGKe-KO mouse showed prolonged time of high glucose level. Immunoblot analysis showed that phosphorylation of novel class protein kinase C (nPKC) is upregulated in white adipose tissue. It is known to be activated by diacylglycerol (DG). HFD is reported to increase DG contents in tissues or organs. Since DGKe-KO mouse is not able to manipulate increased DG adequately, nPKC activation is accelerated. nPKC is key molecule which induces insulin resistance. Present study revealed that insulin resistance is invoked particularly in WAT via acceleration of nPKC in HFD fed DGKe-KO mouse.
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