Moreover, we demonstrated, for the first time, that the PG, similarly to that observed in other organs 31, develops a drastic insulin resistance in conditions of obesity, as demonstrated by the severely reduced increments of AKT phosphorylation in response to an acute insulin injection, thus reinforcing the idea of a relevant crosstalk between the alterations in the endocrine–metabolic status (i.e. obesity) and the dysregulation of the normal metabolic homeostasis of the PG. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.