| Project/Area Number |
16K00877
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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 |
Eating habits
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| Research Institution | Kinjo Gakuin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
那須 民江 中部大学, 生命健康科学部, 特任教授 (10020794)
佐藤 秀一 島根大学, 学術研究院医学・看護学系, 准教授 (10332785)
飛田 博史 島根大学, 学術研究院医学・看護学系, 助教 (60457190)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | NASH / 胆汁酸 / SHRSP5/Dmcr / 線維化 / 脂質 |
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| Outline of Final Research Achievements |
We investigated whether dietary bile acid affected SHRSP5/Dmcr liver damage.
At 10 weeks of age, the male SHRSP5/Dmcr rats were divided equally into 4 groups and fed with HFC diet as follows : Cholic acid (CA) 0% HFC group, CA 0.5% HFC group, CA 2% HFC group, CA 4% HFC group for 8 weeks.Hepatic lesions of SHRSP5/Dmcr progressed by dietary bile acid concentrations. However, the increase of dietary bile acid concentrations decreased body weight and epididymal adipose tissue. The expression of Transmembrane G protein-coupled Receptor5 (TGR5) in brown adipocytes and small intestine was not different in each group with different bile acid levels. Non-obese and steatohepatitis progressin may not be a mechanism via TGR5.
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| Academic Significance and Societal Importance of the Research Achievements |
日本人に多いとされる非肥満型非アルコール性脂肪性肝炎は、食事の組成でその病状が異なる。食事で摂取する胆汁酸の濃度が高くなるにつれ、顕著に肝障害が進行することが明らかになった。
食事に含まれる成分の何が肝臓障害の原因となるのかを明らかにすることは、食習慣の改善に役立つものと考える。これまでの成果と合わせて考察することにより、特定の栄養素だけでなく、栄養素の組合せが問題になることが考えられた。
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