Abstract
The BTBR ob/ob mice (black and tan, obese, tufted) are characterized by a mutation on the leptin gene (Lep ob ) that makes it knockout for this gene. Due to this mutation, BTBR mice show a number of characteristics, such as:hyperfagia, hyperglycemia, glucose intolerance, hyperisulinism,hypertriglyceridemia, impaired healing, albuminuria, hypothermia, andincreased production of pituitary and adrenal hormones. Moreover, theseanimals show a secondary subfertility related to hypogonadotrophichypogonadism because leptin has a direct effect on the central nervous systemthrough the release of the GnRH hormones and, subsequently, the release ofthe luteinizing hormone (LH) and the follicle stimulating hormone (FSH). Severalstrategies were tested with the aim of repairing the fertility of the ob/ob mice,including restricted diets and treatment with recombinant human and mouseleptin. Furthermore, previous literature showed that the fat transplantation was able to repair the fertility of the ob mice, decrease its body weight and increase the blood plasma concentration of leptin. However, most of these articles did not specify how much fat and time is necessary for the transplantation to work. Therefore, it is expected that specifying these methods will increase the pool of BTR ob/ob mice in the laboratory vivarium.
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