| Project/Area Number |
16K12720
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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 |
Eating habits
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| Research Institution | Shizuoka University |
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Principal Investigator |
Yukita Akira 静岡大学, 教育学部, 准教授 (80401214)
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| Co-Investigator(Kenkyū-buntansha) |
茶山 和敏 静岡大学, 農学部, 准教授 (30260582)
中村 浩彰 松本歯科大学, 歯学部, 教授 (50227930)
二宮 禎 日本大学, 歯学部, 准教授 (00360222)
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | CCL25 / 母乳 / 骨形成 / 骨代謝 / ケモカイン / 骨芽細胞 / 破骨細胞 / 乳汁 / 食と栄養 / 食と骨形成 |
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| Outline of Final Research Achievements |
Previous studies have shown that CCL25, which is known to be involved in intestinal immunity, is contained in breast milk. By the artificial lactation experiment we established before, we found that CCL25 in artificial milk can activate bone formation and bone resorption, and promote bone growth in the longitudinal direction of infant mice. On the other hand, although we attempted to extend the period of artificial nursing, it was very difficult to extend the period of 10 days or more. Therefore, we investigated the role of CCL25 in bone tissue using a CCL25 gene-deficient mouse. As a result, although there was no significant difference in skeletal abnormalities and long bone length in both 10-day-old and 10-week-old mice, increase in bone mass was observed in 10-week-old mice.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は腸管免疫に関わるタンパク質であるCCL25が骨の形成にも関わることを初めて示した。特に成獣期において、体内のCCL25が減少すると骨形成が活発になり骨量が増えることから、過剰なCCL25は骨形成の不全や骨量の低下の原因となる可能性が考えらる。さらなる研究が必要ではあるが、CCL25の体内量の調節を介して、全く新しい骨疾患の治療薬が開発できるのではないかと期待している。
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