Binge eating (BE) is often triggered by stress, dieting, and adverse environmental factors, and represents a common precursor to eating disorders such as anorexia, bulimia, and BE disorder. Stress-induced hyperphagia captures core features of binge-like feeding and shares neurobiological substrates will BE disorder, making it a useful behavioral readout for dissecting underlying mechanisms. We used the genetically tractable worm Caenorhabditis elegans to examine how starvation and stress interact to drive feeding, quantifying pharyngeal pumping as a measure of food intake. Combined starvation and heat stress increased feeding beyond starvation alone, with effects shaped by stress timing, food quality, and sex. Feeding phenotypes were separable from locomotor and feeding-capacity defects. Mutations in evolutionarily conserved homeostatic and hedonic feeding-pathway genes showed distinct hyperphagic responses, implicating that conserved neuronal circuits govern stress-induced feeding across species. This model offers a platform for genetic screening and drug testing to accelerate discovery of therapeutics for binge-like feeding disorders.
Stress induced hyperphagia in C. elegans as a genetic model for binge eating disorders
Pucci, Mariangela
;D'Addario, Claudio;
2026-01-01
Abstract
Binge eating (BE) is often triggered by stress, dieting, and adverse environmental factors, and represents a common precursor to eating disorders such as anorexia, bulimia, and BE disorder. Stress-induced hyperphagia captures core features of binge-like feeding and shares neurobiological substrates will BE disorder, making it a useful behavioral readout for dissecting underlying mechanisms. We used the genetically tractable worm Caenorhabditis elegans to examine how starvation and stress interact to drive feeding, quantifying pharyngeal pumping as a measure of food intake. Combined starvation and heat stress increased feeding beyond starvation alone, with effects shaped by stress timing, food quality, and sex. Feeding phenotypes were separable from locomotor and feeding-capacity defects. Mutations in evolutionarily conserved homeostatic and hedonic feeding-pathway genes showed distinct hyperphagic responses, implicating that conserved neuronal circuits govern stress-induced feeding across species. This model offers a platform for genetic screening and drug testing to accelerate discovery of therapeutics for binge-like feeding disorders.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


