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Genetic disruption of the Gipr in Apoe / mice promotes atherosclerosis

Experiments in islet cell models have shown that intracellular signalling after GLP-1R agonist binding occurs via two pathways, one of which (cyclic adenosine monophosphate generation) enhances insulin release, while the other (-arrestin recruitment) causes GLP-1R receptor internalisation, and hence reduces cellular sensitivity to ligand

Neither renal composite 1 (40% eGFR decline, RRT, or renal death) nor composite 2 (composite 1 variables plus macroalbuminuria) was reduced by exenatide in unadjusted analyses

*Correspondence: Jens Juul Holst [email protected] This article was submitted to Molecular and Structural Endocrinology, a section of the journal Frontiers in Endocrinology Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers