In all, the above-mentioned relationships between PrAO-dependent methylamine oxidation, adipocyte metabolism, and glucose or lipid handling deserve to be further studied in pathologies such as diabetes or obesity At the present time, inhibition of PrAO activity, either of a pathological or pharmacological nature, should be associated with a limitation of the somewhat insulin-like actions of methylamine and does not appear as a so attractive way of treating metabolic diseases as recently proposed [32]. This evidence concerns the gene INS and metabolic disease.