AMPK-dependent regulation of GLP1 expression in L-like cells

    1. Geyang Xu1
    1. 1Department of Physiology, School of Medicine, Jinan University, Guangzhou, Guangdong, China
    2. 2Endoscopy Center, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China
    3. 3Shenzhen University Diabetes Center, Shenzhen University Health Science Center, Shenzhen, Guangdong, China
    4. 4Department of Surgery, University of Michigan Medical Center, Ann Arbor, Michigan, USA
    1. Correspondence should be addressed to W Zhang or G Xu; Email: weizhenz{at} or xugeyangliang{at}


    This study examined whether AMPK, an evolutionarily conserved sensor of cellular energy status, determines the production of glucagon-like peptide-1 (GLP1). A negative relation existed between phosphorylation of AMPKα and the expression and secretion of GLP1 during changes in energy status in STC-1 cells, an L-like cell line. High concentration of glucose (25 mmol/L) decreased AMPKα phosphorylation, whereas it stimulated the expression and secretion of GLP1 relative to 5.6 mmol/L glucose. Serum starvation upregulated AMPKα phosphorylation, whereas it reduced GLP1 production significantly. Stimulation of AMPK phosphorylation by AICAR and overexpression of wild-type AMPKα1, constitutively active AMPKα1 plasmids, or AMPKα1 lentivirus particles suppressed proglucagon mRNA and protein contents in STC-1 cells. Inactivation of AMPK by Compound C, AMPKα1 siRNA or kinase-inactive AMPKα1 mutant increased the expression and secretion of GLP1. Our results suggest that AMPKα1 may link energy supply with the production of GLP1 in L-like cells.

    • Received 17 July 2016
    • Accepted 4 August 2016
    • Made available online as an Accepted Preprint 4 August 2016
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