However, when LEPR was in vivo abrogated in proopiomelanocortin (POMC) neurons of ARCs, which are well-known to foster fullness and satiety responses, mice developed mild obesity, hyperleptinaemia and glucose intolerance without changes in food consumption or EE [43,44,45,46,47,48]. This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.