The mechanism of diet-induced thermogenesity in brown adipsose tissue for the increase in energy expenditure
| Project/Area Number |
16K01855
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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 |
Applied health science
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| Research Institution | National Institutes of Biomedical Innovation, Health and Nutrition |
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Principal Investigator |
Yamazaki Tomomi 国立研究開発法人医薬基盤・健康・栄養研究所, 国立健康・栄養研究所 臨床栄養研究部, 山崎聖美 (00218439)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 食事誘発性熱産生 / エネルギー代謝 / 褐色脂肪組織 / PPARα / 時計遺伝子 / UCP1 / メタボリックシンドローム / 肥満 |
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| Outline of Final Research Achievements |
A system to analyze diet-induced thermogenesis (DIT) from protein, carbohydrate, and lipid using mice was built. DIT from protein, carbohydrate, and lipid varied according to mouse strains. It was thought that a difference in activity of mitochondrial uncoupling protein UCP1 of the brown adipose tissue contributed to these differences. DIT was observed even in PPARα knockout mice, and the mitochondrial activity and the level of UCP1 protein were at the same level as wild type mice. Then, after giving fenofibrate to mice, DIT increased to double from 10% to 20% of energy that they took in with the wild type mice, but the increase was not seen in the PPARα knockout mice.
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| Academic Significance and Societal Importance of the Research Achievements |
マウスを用いた食事誘発性熱産生の増加に関しては、体温上昇やエネルギー消費量上昇が指標にされていたが、本研究により構築された測定系により増加率が算出可能となった。これにより、様々な食品成分による食事誘発性熱産生亢進に関する詳細な研究が可能になると期待される。
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Report
(4 results)
Research Products
(29 results)
