2022 Fiscal Year Final Research Report
Establishment of a model for progression from non-alcoholic steatohepatitis (NASH) to hepatocellular carcinoma induced by dietary factors alone
Project/Area Number |
20K11567
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 59040:Nutrition science and health science-related
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Research Institution | Kinjo Gakuin University |
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, 客員教授 (10020794)
飛田 博史 島根大学, 学術研究院医学・看護学系, 講師 (60457190)
安井 菜穂美 武庫川女子大学, 薬学部, 講師 (70399145)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 食事因子 / NASH / 肝癌 / SHRSP5/Dmcr |
Outline of Final Research Achievements |
Models of progression from NASH to hepatocellular carcinoma by dietary factors alone are widely desired. Therefore, the aim of this study was to “Establishment of a model for progression from non-alcoholic steatohepatitis (NASH) to hepatocellular carcinoma induced by dietary factors alone”. SHRSP5/Dmcr, which induces NASH in high-fat, high-cholesterol (HFC) diets, were fed iron for 24 weeks. The results showed that iron intake confirmed the progression of liver inflammation. However, liver damage was mild and did not progress to liver cancer. To tolerate long-term feeding, the base diet was 1/2 HFC, which showed inflammation after 8 weeks of consumption. It was suggested that liver damage did not progress over time at low HFC concentrations, which could be the cause of the less severe liver damage.
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Free Research Field |
栄養学
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Academic Significance and Societal Importance of the Research Achievements |
食事因子のみで非アルコール性脂肪性肝炎から肝癌へ進行するモデルは存在しない。疾病の予防や治療の研究にはモデルが必要である。今回の研究で、鉄の摂取は肝臓の炎症を重症化することが示唆された。また、HFC飼料濃度が低い場合、短期間では肝障害が発症しても、長期的では肝障害が重症化しないことが示唆された。モデル作成の一助となる知見が得られた。
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