Interestingly, in vitro mechanistic studies suggest the peptide is biased towards the GIPR, activating with equipotency to native GIP whilst having 5-fold weaker affinity than native GLP-1 at GLP-1R, with a preference to initiate cAMP mobilisation to enhance insulin secretion (317), which may be of particular benefit in obesity-diabetes. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.