Regulatory mechanism of intestinalization of gastric mucosa by leptin receptor signaling
| Project/Area Number |
17K08790
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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 |
Experimental pathology
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| Research Institution | Prefectural University of Hiroshima |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 胃 / レプチン / 胃がん / 腸上皮化生 / 高脂肪食 / 食事性肥満 / 食餌性肥満 / 肥満 |
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| Outline of Final Research Achievements |
Dysregulation of leptin receptor (LepR) signaling links to development of gastric tumors. In this study, we demonstrated that LepR signaling activation is essential for the induction of gastric tumor, intestinal metaplasia and dysbiosis of microbiota using both models of gene-targeting and high-fat diet-induced obese mice. LepR-deletion suppresses the development of these pathogenesis and dysbiosis. These results indicate that the gastric leptin signaling can regulate cell differentiation of the stomach and environment of gastric mucosa.
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| Academic Significance and Societal Importance of the Research Achievements |
これまでレプチンの研究は、レプチンによるエネルギー代謝調節とその破綻機構に焦点が当てられ、胃で産生されるレプチンの胃局所における調節作用はほとんど明らかになっていない。本研究は、消化管特異的なレプチンシグナルに焦点をあて作製された遺伝子改変マウスを用いており、それ故、研究成果はヒト腸上皮化生、胃がん発症機構の解明においても重要な情報になりうる。
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Report
(4 results)
Research Products
(8 results)
