The genetic basis for this inbred mouse model is a single-gene autosomal recessive defect in leptin receptor which produces leptin resistance and results in hyperphagia, obesity and the subsequent symptoms of insulin resistance, insufficient insulin secretion, hyperglycemia and elevated HbA1c (9.1±2.1) levels [22], [41], [42], [43]. This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.