The Lepr gene encodes the leptin receptor (LEPR), a transmembrane protein that plays a critical role in regulating energy balance, metabolism, and neuroendocrine functions by binding leptin, a hormone secreted by adipocytes. This gene is expressed in multiple tissues, including the hypothalamus (particularly the arcuate nucleus), liver, pancreas, and immune cells, and mediates leptin signaling through the JAK-STAT pathway. The Lepr-CreERT2 mice are constructed by integrating a tamoxifen-inducible CreERT2 recombinase expression cassette into the endogenous Lepr gene via gene editing technology. Without tamoxifen treatment, CreERT2 recombinase primarily resides in the cytoplasm; nuclear translocation and recombination activity of CreERT2 only occur upon tamoxifen stimulation. When Lepr-CreERT2 mice are crossed with mice containing loxP sites, tamoxifen induction triggers Cre recombinase-mediated sequence recombination between loxP sites in leptin receptor-expressing cells of the offspring.