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Aims Diabetes impairs insulin‐induced endothelium‐dependent relaxation by reducing nitric oxide (NO) production. GLP‐1, an incretin hormone, has been shown to prevent the development of endothelial dysfunction. In this study, we hypothesized that GLP‐1 would improve the impaired insulin‐induced relaxation response in diabetic mice. We also examined the underlying mechanisms. Methods Using aortic rings from ob/ob mice, an animal model of obesity and type 2 diabetes, and from lean mice, vascular relaxation responses and protein expressions were evaluated using insulin, GLP‐1, and pathway‐specific inhibitors to elucidate the mechanisms of response. In parallel experiments, β‐arrestin2 siRNA‐transfected aortas were treated with GLP‐1 to evaluate its effects on aortic response pathways. Results When compared to that of untreated ob/ob aortas, GLP‐1 increased insulin‐induced vasorelaxation and NO production. AMPK inhibition did not alter this vasorelaxation in both GLP‐1‐treated lean and ob/ob aortas, while Akt inhibition reduced vasorelaxation in both groups, and co‐treatment with GLP‐1 and insulin caused Akt/eNOS activation. Additionally, GLP‐1 decreased GRK2 activity and enhanced β‐arrestin2 translocation from the cytosol to membrane in ob/ob aortas. β‐Arrestin2 siRNA decreased insulin‐induced relaxation both in lean aortas and GLP‐1‐treated ob/ob aortas. Conclusions We demonstrated that insulin‐induced relaxation is dependent on β‐arrestin2 translocation and Akt activation via GLP‐1‐stimulated GRK2 inactivation in ob/ob aortas. We showed a novel cross‐talk between GLP‐1‐responsive β‐arrestin2 and insulin signalling in diabetic aortas.