Journal
CELL REPORTS
Volume 21, Issue 9, Pages 2628-2638Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.10.113
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Funding
- JSPS KAKENHI [16K19391, 15H02397, 15H05949, 16H06280]
- CREST [JPMJCR1654]
- Nakatani Foundation
- Grants-in-Aid for Scientific Research [16K19391, 15H02397] Funding Source: KAKEN
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AMP-activated protein kinase (AMPK), a master regulator of cellular metabolism, is a potential target for type 2 diabetes. Although extensive in vitro studies have revealed the complex regulation of AMPK, much remains unknown about the regulation in vivo. We therefore developed transgenic mice expressing a highly sensitive fluorescence resonance energy transfer (FRET)-based biosensor for AMPK, called AMPKAR-EV. AMPKAR-EV allowed us to readily examine the role of LKB1, a canonical stimulator of AMPK, in drug-induced activation and inactivation of AMPK in vitro. In transgenic mice expressing AMPKAR-EV, the AMP analog AICAR activated AMPK in muscle. In contrast, the antidiabetic drug metformin activated AMPK in liver, highlighting the organ-specific action of AMPK stimulators. Moreover, we found that AMPK was activated primarily in fast-twitch muscle fibers after tetanic contraction and exercise. These observations suggest that the AMPKAR-EV mouse will pave a way to understanding the heterogeneous responses of AMPK among cell types in vivo.
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