| Project/Area Number |
16K15330
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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 |
Laboratory medicine
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
長谷川 浩司 福島県立医科大学, 医学部, 講師 (50443867)
蔵野 信 東京大学, 医学部附属病院, 講師 (60621745)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | アポ蛋白D / 慢性炎症 / 糖尿病 / インスリン抵抗性 / 糖尿病合併症 / 2型糖尿病 |
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| Outline of Final Research Achievements |
The expression of apoD in adipose tissue increased in the DIO mice compared with the wild type mice; on the other hand, the apoD expression decreased with the differentiation of 3T3L1 cells. Over-expression of apoD in mice resulted in the amelioration of insulin resistance, which was accompanied by the suppression of inflammatory cytokines. The LPS induced inflammation, examined in vivo and in vitro, was also suppressed with the abundant apoD protein. Two clinical cross-sectional studies revealed that plasma apoD level correlated negatively with the inflammatory cytokine levels and clinical data associated with insulin resistance, and positively associated with anti-inflammatory cytokine levels and clinical data associated with insulin sensitivity. Thus, we can propose that increased plasma apoD level would be a marker of anti-inflammatory condition and insulin sensitive state, and apoD protein might possess the function of suppressing inflammation and insulin resistance.
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