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Vorinostat suppresses hypoxia signaling by modulating nuclear translocation of hypoxia inducible factor 1 alpha

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While the contributions of alpha-cell GLP-1 versus glucagon to the regulation of beta-cell function have yet to be established, these findings illustrate that beta-cell GLP-1R stimulation is primarily mediated by paracrine intra-islet ligands, rather than by the endocrine action of gut-derived GLP-1