Not only is the obesity phenotype of KOGlp1r mice more prominent than the reported phenotypes for mice lacking Lepr in Pomc or Agrp neurons since early development (9, 10, 41), but KOGlp1r mice do not exhibit the alterations in glucose homeostasis and/or energy expenditure displayed by these other models. This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.