期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 290, 期 6, 页码 3793-3802出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M114.604421
关键词
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资金
- NIDDK, National Institutes of Health [R00DK085142, R01DK63349]
- JHU-UMD Diabetes Research Center [P60DK079637]
Metformin is the most widely prescribed oral anti-diabetic agent. Recently, we have shown that low metformin concentrations found in the portal vein suppress glucose production in hepatocytes through activation of AMPK. Moreover, low concentrations of metformin were found to activate AMPK by increasing the phosphorylation of AMPK alpha at Thr-172. However, the mechanism underlying the increase in AMPK alpha phosphorylation at Thr-172 and activation by metformin remains unknown. In the current study, we find that low concentrations of metformin promote the formation of the AMPK alpha beta gamma complex, resulting in an increase in net phosphorylation of the AMPK alpha catalytic subunit at Thr-172 by augmenting phosphorylation by LKB1 and antagonizing dephosphorylation by PP2C.
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