| Project/Area Number |
17K15977
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Kochi University (2019-2020)
Okayama University (2018)
University of Occupational and Environmental Health, Japan (2017) |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 脂肪性肝疾患 / オートファジー / 酸化ストレス / HO-1 / 飽和脂肪酸 / 肝細胞 / 遊離脂肪酸 / 肝臓 / カルシウム / 肝細胞癌 / オートファジ― / 慢性肝疾患 |
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| Outline of Final Research Achievements |
Saturated fatty acids inhibit autophagy in the liver, whereas unsaturated fatty acids improve it. Experiments in cultured cells have shown that this effect is related to the ability of hepatocytes to regulate calcium levels in the sarcoplasmic reticulum. This was published in the international journal Experimental Cell Research. In addition, when the concentration of saturated fatty acids in the blood was increased in vivo, only HO-1, an oxidative stress-related enzyme, was found to be upregulated in the liver of mice treated intravenously with saturated fatty acids. In experiments on cultured cells, we found that HO-1 reduces the oxidative stress induced by saturated fatty acids. These results have been published in the international journal Nutrients.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究結果は、特に脂肪性肝疾患における飽和脂肪酸の脂肪毒性の分子機序の一部を説明するものであり、飽和脂肪酸がもたらすオートファジーの障害には小胞体内カルシウム調整機構が、酸化ストレスにはHO-1が重要な役割を持つ可能性が確認されました。脂肪性肝疾患に対する治療薬はいまだに少なく、その病態の促進要因も明らかにはなっていません。今回の研究で確認された機序を標的とした新たな治療への応用が期待されます。
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