Loss of function mutations in leptin (ob/ob) and leptin receptor (db/db) provide insight into β‐cell physiology in nondiabetic‐obese and diabetic‐obese states within individual mouse strains (Bock, Pakkenberg, & Buschard, 2003; Butler et al., 2003; Hummel, Coleman, & Lane, 1972; Keller et al., 2008; Leiter, Coleman, Eisenstein, & Strack, 1980); however, leptin and its receptor play a critical role in β‐cell function independent of obesity, limiting interpretations of these studies (Covey et al., 2006). Here, LEP is linked to obesity due to melanocortin 4 receptor deficiency.