The investigation of mechanisms on the regulation of AMPK activation mediated by LKB1 translocation in hypothalamus

• Project/Area Number: 20790653
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Single-year Grants
• Research Field: Metabolomics
• Research Institution: Kumamoto University
• Principal Investigator: KAWASHIMA Junji Kumamoto University, 医学部附属病院, 特任助教 (70467984)
• Project Period (FY): 2008 – 2009
• Project Status: Completed (Fiscal Year 2009)
• Budget Amount: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000); Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000); Fiscal Year 2008: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
• Keywords: エネルギー / 糖質代謝異常 / LKB1 / AMPK / 視床下部

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.