2017 Fiscal Year Final Research Report
Investigation of down regulation mechanism of Lect2 gene expression by metformin
| Project/Area Number |
15K19509
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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 |
Metabolomics
|
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Keywords | Lect2 / Metformin / AMPK / PKA |
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| Outline of Final Research Achievements |
A hepatokine leukocyte cell-derived chemotaxin 2（LECT2）which is overproduced with obesity cause insulin resistance in skeletal muscle. It is expected that suppression of LECT2 production is a new therapeutic target of insulin resistance, but no drug is known which lowering LECT2 production to date. Here I revealed that an oral anti-diabetic drug metformin can suppress Lect2 gene expression via AMPK activation in cultured hepatocyte. This pathway may relate RNA instability mechanism because metformin did not alter LECT2 promoter activity. Further experiment is needed to understand the molecular mechanism in this pathway much more.
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| Free Research Field |
分子生物学
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