| Project/Area Number |
23659464
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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 |
Metabolomics
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YATOH Shigeru 筑波大学, 医学医療系, 講師 (50451703)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 脂肪酸 / 嗜好性 / 糖尿病 |
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| Research Abstract |
In this study, we investigated the effects of Elovl6 deletion in leptin receptor-deficient db/db mice, a model of type 2 diabetes. We analyzed the body weights, serum glucose, insulin and HbA1c levels of db+/m, db/db, and db/db-Elovl6KO mice. We also performed immunohistochemical staining and quantitative RT-PCR analysis of islet.Although the obesity of db/db-Elovl6KO mice was similar to db/db mice, development of hyperglycemia and glucose intolerance was dramatically improved. Histological examination indicated that Elovl6 deletion was associated with increased islet mass in db/db mice, and this correlated with serum hyperinsulinemia and glucose-responsive insulin secretion. The expression of several inflammatory genes such as TNF-α and MCP-1 were reduced, and the expression of genes related to β cell function such as PDX-1 and insulin were increased in islets from db/db-Elovl6KO mice compared with db/dbmice. These results suggest that Elovl6 is an important factor on both beta-cell mass and function in T2D. Elovl6 inhibition can be a novel therapeutic target for T2D.
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