AMPK-dependent regulation of GLP1 expression in L-like cells
AMPK-dependent regulation of GLP1 expression in L-like cells
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L 样细胞中 GLP1 表达的 AMPK 依赖性调节
DOI：
10.1530/jme-16-0099
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发表时间：
2016-10-01
影响因子：
3.5
通讯作者：
Xu, Geyang
中科院分区：
文献类型：
--
作者：
Jiang, Sushi;Zhai, Hening;Xu, Geyang
本研究检测AMPK，一种进化上保守的细胞能量状态传感器，是否决定胰高血糖素样肽-1（GLP 1）的产生。在L样细胞系STC-1细胞能量状态变化过程中，AMPK α的磷酸化与GLP 1的表达和分泌呈负相关。高浓度葡萄糖（25 mmol/L）降低AMPK α磷酸化水平，而相对于5.6 mmol/L葡萄糖，高浓度葡萄糖刺激GLP 1的表达和分泌。血清饥饿上调AMPK α磷酸化，而它减少GLP 1的生产显着。AICAR对AMPK磷酸化的刺激和野生型AMPK α 1、组成型活性AMPK α 1质粒或AMPK α 1慢病毒颗粒的过表达抑制STC-1细胞中胰高血糖素原mRNA和蛋白质含量。通过化合物C、AMPK α 1 siRNA或激酶失活的AMPK α 1突变体使AMPK失活增加GLP 1的表达和分泌。我们的研究结果表明，AMPK α 1可能与L-样细胞中GLP 1的产生有关。
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 AMPK alpha 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 AMPK alpha phosphorylation, whereas it stimulated the expression and secretion of GLP1 relative to 5.6 mmol/L glucose. Serum starvation upregulated AMPK alpha phosphorylation, whereas it reduced GLP1 production significantly. Stimulation of AMPK phosphorylation by AICAR and overexpression of wild-type AMPK alpha 1, constitutively active AMPK alpha 1 plasmids, or AMPK alpha 1 lentivirus particles suppressed proglucagon mRNA and protein contents in STC-1 cells. Inactivation of AMPK by Compound C, AMPK alpha 1 siRNA or kinase-inactive AMPK alpha 1 mutant increased the expression and secretion of GLP1. Our results suggest that AMPK alpha 1 may link energy supply with the production of GLP1 in L-like cells.