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In 1997, a mouse study demonstrated that genetic ablation of Mc4r resulted in an obese phenotype, hyperphagia, and hyperinsulinemia ( Mc3r knockout mice exhibit increased adiposity without developing overt obesity and, in some cases, display hypophagia ( Mc3r / Mc4r double knockout mice develop a more severe obese phenotype than Mc4r knockout animals alone, indicating that the two receptors exert non-redundant effects on energy homeostasis ( In line with these observations in rodents, human genetic studies published in the early 2000s identified MC4R mutations as the most common monogenic cause of obesity, affecting up to 6% of individuals with severe obesity ( MC3R mutations were reported in fewer than 2% of obese individuals ( In parallel with emerging genetic evidence, early pharmacological studies using MC3R-selective ligands, including -MSH and synthetic analogues, further shaped receptor prioritization within the MC system ( While these studies emphasized the role of MC4R in regulating metabolism, later research implicates both MC3R and MC4R in modulation of food intake and body weight