Using novel LUXendins, we were able to perform unprecedented experiments and reveal new biology regarding GLP1R. As the best performing dye, LUXendin551 allowed GLP1R and thus beta cells to be reported in intravital experiments of a type 1 diabetes preclinical mouse model, which is not amenable to further genetic manipulation. Such experiments are important, since we are still lacking information on the changes that occur in beta cell mass (and GLP1R expression) during the insulitis and autoimmune destruction . To allow noninvasive imaging, Cy7 was installed on the LUXendin backbone to produce LUXendin762, a near-infrared probe. We were able to demonstrate that LUXendin762 signal can be recorded in vivo (compared to saline-treated controls) and sequesters in organs known to express the GLP1R such as the pancreas and brain . Of interest, LUXendin762 highlighted differential access routes to peripheral and brain GLP1R sites, with subcutaneous and not intraperitoneal injection labelling the latter. While the mechanisms are currently unknown, we speculate that ligand injected subcutaneously is less prone to the first pass effect and as such is able to abundantly enter the carotid arteries for entry into the brain. LUXendin762 thus opens up for the first time non-invasive longitudinal studies of GLP1R in mice using readily accessible platforms available in most academic/industrial animal facilities. Such studies are particularly pertinent, since GLP1R is also a readout for beta cell mass in preclinical models of type 2 diabetes and other metabolic syndromes . Furthermore, longitudinal measures in the same animal are statistically more powerful and refined compared to assessment of various timepoints in multiple cohorts.