Thus, deletion of a single Tcf7l2 allele led to impaired tolerance of glucose administrated intraperitoneally, and generated distinct features of obesity-induced glucose intolerance, while biallelic Tcf7l2 deletion impacted on the oral glucose tolerance, it might exert an effect through endocrine signalling molecules such as the incretins. This evidence concerns the gene TCF7L2 and obesity due to melanocortin 4 receptor deficiency.