The glucagon-like peptide-1 receptor (GLP1R) is a class B G protein-coupled receptor involved in the regulation of glucose homeostasis, food intake and inflammation . As such, GLP1R agonist (GLP1RA) therapy has become a mainstay of type 2 diabetes treatment during the past decade, with a number of drugs on the market based upon stabilized analogs of glucagon-like peptide-1 . Most recently, phase III trials of the third generation semaglutide have shown a ~15% reduction in body weight when combined with lifestyle interventions , leading to approval of GLP1RA as the first non-surgical treatment for complex obesity. Despite this, information concerning the localization of GLP1R is lacking, primarily due to the paucity of reliable and specific reagents for its detection and visualization . Without this knowledge, it is difficult to elucidate the exact cellular mechanisms underlying GLP1R actions, many of which could be key to developing even more specific or effective treatments for metabolic/inflammatory disease states, by for instance tissue-targeted delivery . For example, GLP1RA have been shown to reduce the progression from non-alcoholic fatty liver disease/non-alcoholic steatohepatitis to fulminant fibrosis , yet where and how the GLP1R acts is currently uncertain. Along similar lines, GLP1RA exert inhibitory (and beneficial) effects on glucagon secretion, yet pancreatic GLP1R distribution and signaling remain debated . Lastly, the neural circuits that GLP1RA are able to access to exert effects on food intake remain to be fully delineated .