The leptin (LEP) gene, also known as the OB gene, encodes the leptin protein, which is secreted into the circulation by white adipocytes and plays a major role in the regulation of energy homeostasis. Circulating leptin binds to leptin receptors (LEPR) in the brain, activating downstream signaling pathways that inhibit feeding and promote energy expenditure. Leptin also has multiple endocrine functions and is involved in physiopathological processes such as immune and inflammatory responses, hematopoiesis, angiogenesis, reproduction, bone formation, and wound healing ^[1]. Mutations in the LEP gene and its regulatory regions lead to severe obesity and morbid obesity with hypogonadism in humans and are also associated with the development of type II diabetes ^[2].

This strain is a Lep deletion mouse model that uses gene editing technology to knock out the expression of human LEP gene homolog in mice with impaired leptin synthesis. According to the literature, this mouse model exhibits obesity, excessive food intake, transient hyperglycemia, poor glucose tolerance, and elevated plasma insulin, accompanied by hypometabolism, hypothermia, and low fertility, in addition to impaired wound healing and increased production of hormones by their pituitary and adrenal glands ^[3]; The phenotype is more similar to that of type II diabetes and obesity in stages I and II, with an increase in the number and size are increased, which can be used in obesity and type II diabetes studies. Homozygous Lep KO mice are viable but the females are sterile and the males have reduced fecundity.