2009 Fiscal Year Final Research Report
The investigation of mechanisms on the regulation of AMPK activation mediated by LKB1 translocation in hypothalamus
| Project/Area Number |
20790653
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | Kumamoto University |
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Principal Investigator |
KAWASHIMA Junji Kumamoto University, 医学部附属病院, 特任助教 (70467984)
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| Project Period (FY) |
2008 – 2009
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| Keywords | エネルギー / 糖質代謝異常 |
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| Research Abstract |
LKB1 expression was recognized by immunohistochemistry (IHC) using the anti-LKB1 antibody (Ley37D) in HeLa cells which LKB1 are overexpressed. AMPK phosphorylation (Thr^<172>) in re-fed mice was suppressed in liver, compared to fasted mice. However, it was difficult to recognize LKB1 localization in liver by IHC using anti-LKB1 antibodies (Ley37D or D-19). 2-deoxy-D-glucose (2DG) or AICAR (an AMPK activator) markedly increased AMPK phosphorylation (Thr^<172>) in N43/5 cells, which are POMC expressing hypothalamic neurons. 2DG or AICAR also induced LKB1 translocation from nuclear to cytoplasm.
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