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We suspect that metabolic/bioenergetic reprograming, observed in this study, could also mediate short-term maintenance of -cell function upon withdrawal of GLP-1 analogues, as documented in humans and rodents by others 21, 33
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Additionally, while both laboratory and prescription dispensing data are captured in Optum CDM, indication information was not available and data were generated from healthcare delivery rather than for research purposes and may therefore be incomplete or missing
The key insulinotropic actions of GLP-1 via the class B1 G-protein-coupled receptor (GPCR) are exerted by cyclic adenosine monophosphate (cAMP) formation, which, in conjunction with increased Ca 2+ levels, promotes exocytosis of insulin-containing vesicles [39]
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