Elucidation of the mechanism of VEGF-B signal-regulated fatty acid uptake in hepatocytes
| Project/Area Number |
17K15963
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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 | Wakayama Medical University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ランソプラゾール / VEGF-B / 脂肪肝 / NAFLD / 脂質 / NASH |
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| Outline of Final Research Achievements |
Lansoprazole reduced the expression of VEGF-B mRNA in HepG2 and Hep3B human hepatic cell lines. Some fatty acid transporters were also downregulated by lansoprazole. We investigated the effect of lansoprazole on intracellular lipid accumulation using HepG2 and Hep3B. There was no significant difference in the intracellular fatty acid uptake levels, whereas a marked increase in LDL-cholesterol uptake by lansoprazole. We observed that lansoprazole activated the Liver X receptor (LXR) that is a key transcriptional regulator of cholesterol metabolism in HepG2 and Hep3B cells.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、胃酸分泌抑制剤であるランソプラゾールが肝細胞の脂質代謝機能に与える影響を明らかにした。我々は以前、ランソプラゾールが非アルコール性脂肪肝疾患（NAFLD）モデルラットの病態進行を遅延させるという新しい薬効の存在を報告しており、本研究成果はランソプラゾールによる脂肪肝抑制メカニズムの一つとして重要な知見となった。NAFLDはメタボリック症候群の原因として知られているが、現時点では脂肪肝を解消する有効な治療薬はなく、ランソプラゾールは有用な脂肪肝治療薬候補と考えられる。
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Report
(3 results)
Research Products
(16 results)
