Beta-Endorphin Peptide Drives Binge Eating and Food Reward, While Enkephalin Plays Minimal Role

Male knockout mice lacking either mu-opioid receptors, beta-endorphin, or enkephalin were compared with their wildtype littermates. They were tested for regular and high-fat diet intake, binge eating (measured on re-exposure to HFD after abstinence), food reward (conditioned place preference with HFD), and food devaluation (reduced chow intake after HFD exposure).

Binge eating disorder affects millions of people and has limited pharmacological treatment options. Identifying beta-endorphin as the specific opioid peptide driving binge eating and food reward, distinct from enkephalin, provides a precise molecular target for developing treatments that could reduce pathological overeating without broadly disrupting the opioid system.

The endogenous opioid peptide system has long been implicated in eating disorders and food addiction. This study provides the clearest evidence yet that beta-endorphin, not enkephalin, is the critical peptide mediating the rewarding properties of food and binge eating. This specificity could guide the development of more targeted therapies for binge eating disorder.

The study was conducted in male mice only; female mice, who have higher rates of binge eating disorders in humans, were not tested. Genetic knockouts eliminate the peptide from birth, which may trigger compensatory mechanisms not present in adult pharmacological interventions. The high-fat diet model may not fully capture the complexity of human binge eating disorder.