These data, along with the fact that BKS mice homozygous for the leptin receptor mutation (Leprdb/db) exhibit sural and sciatic NCV deficits by 16 weeks (Ii et al., 2005; Wang et al., 2011; Kan et al., 2012; Hur et al., 2015), may suggest that genetic disruption of leptin signaling is required for large-fiber dysfunction, independent of obesity. This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.