Mice lacking NAPE-PLD in adipocytes spontaneously developed obesity, insulin resistance and inflammation on a normal caloric diet and were more sensitive to high-fat diet-induced metabolic disorders.122 The adipocyte-specific deletion of NAPE-PLD decreased the thermogenic programme (ie, browning/beiging) in adipose tissue and resulted in a profound shift in the gut microbiota composition. The gene discussed is NAPEPLD; the disease is obesity due to melanocortin 4 receptor deficiency.