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Appetite-Related Gut Peptides in Obesity and Binge Eating Disorder

NY Obesity Research Center, St Luke's-Roosevelt Hospital, Columbia University College of Physicians and Surgeons, New York, New York, ag58{at}columbia.edu

Christopher N. Ochner, PhD

NY Obesity Research Center, St Luke's-Roosevelt Hospital, Columbia University College of Physicians and Surgeons, New York, New York

Roni Aviram-Friedman, BS

NY Obesity Research Center, St Luke's-Roosevelt Hospital, Columbia University College of Physicians and Surgeons, New York, New York

The worldwide increase in obesity prevalence is a result of positive energy balance, with energy intake exceeding expenditure. The eating behavior in obesity ranges from mild passive overconsumption to excessive overeating with loss of control observed in binge eating disorder (BED). The signaling systems that underlie appetite control in BED are complex and, at this point, not well understood. The present review highlights the current knowledge of key components of the gut peptide system and examines evidence of defects in signaling that differentiate obese binge eaters from obese non—binge eaters. The signaling network underlying hunger, satiety, and metabolic status includes leptin and insulin from energy stores and cholecystokinin, glucagon-like peptide-1, peptide YY(3-36), and ghrelin from the gastrointestinal tract. Of the many gastrointestinal peptides, ghrelin is the only established appetite-stimulating one, whereas cholecystokinin, glucagon-like peptide-1, and peptide YY(3-36) promote satiety. Adipose tissue provides hormonal signals via leptin and insulin to the brain about energy stores and likely from adiponectin and resistin. Binge eating has been related to a dysfunction in the ghrelin signaling system. Moreover, the larger gastric capacity observed in BED may further reduce satiety signals and contribute to overeating.

Key Words: obesity • binge • eating • BED • hormones • appetite • peptide • ghrelin • CCK • leptin

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