| Project/Area Number |
18K15775
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53010:Gastroenterology-related
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2020: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 非ウイルス性脂肪性肝炎 / メラノコルチン4受容体 / NASHモデルマウス / 非アルコール性脂肪性肝炎 / ４型メラノコルチン受容体 / 肝癌 / 部分肝切除 / Maid遺伝子 |
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| Outline of Final Research Achievements |
The mean body weights of melanocortin-4 receptor (MC4R) and Maid gene-double knockout (DKO) mice and MC4R gene-single knockout (MC4R-KO) mice with regular diet were 66.3g and 36.8g, respectively (P<0.001). Although DKO mice showed a higher degree of visceral fat accumulation than MC4R-KO mice, hepatic fat deposition of DKO mice was similar to that of MC4R-KO mice. Furthermore, there was no evidence of liver cirrhosis and hepatocellular carcinoma even at 52 weeks of age in both knockout mice. These results indicate that Maid gene deletion increases fat accumulation in adipocytes of MC4R gene-deficient mice, but does not increase ectopic fat accumulation in the liver.
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| Academic Significance and Societal Importance of the Research Achievements |
Maid遺伝子は癌化や炎症に関係し、肝癌の発症にも関わることが知られているが、現在までのところ解明されていない部分も多い。本研究において脂肪細胞に作用し、脂肪蓄積を増加させうるという、今まで知られていなかった表現型に関与することが明らかとなった。MC4R,Maid両遺伝子欠損マウスは異所性の脂肪蓄積を悪化させない生理的な肥満であり、この機序の解明は肥満症の病態解明及び治療に有用である可能性がある。
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