Although most of the genetic or genetically modified models of diabetic neuropathy or PDN discussed in this review are suitable for studying the pathogenesis of the diseases, the C57BL/Ks (db/db) mice, streptozotocin-induced C57BL6/J and ddY mice, spontaneously diabetic WBN/Kob rats, nonobese diabetic mice, spontaneously induced Ins2 Akita mice, and leptin-deficient (ob/ob) mice have been found as better models for human diabetic neuropathy when high-fat diet-fed female C57BL6/J mice have been suggested to use for prediabetic or obesity related diabetic neuropathy. Here, LEP is linked to obesity due to melanocortin 4 receptor deficiency.