Review article: the gastrointestinal tract: neuroendocrine regulation of satiety and food intake


  • Conflicts of interest:
    The authors have declared no conflicts of interest.

  • This article appeared as part of a supplement sponsored by Nycomed bv.

Dr J. Maljaars, Division of Gastroenterology–Hepatology, Department of Internal Medicine, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands.


Background  The gastrointestinal tract elicits numerous signals regulating food intake and satiety, and recently many studies have been performed to elucidate the mechanisms regulating these signals.

Aim  To describe the effects of the gastrointestinal tract on satiety, satiation and food intake.

Methods  A PubMed search was performed to identify and select the relevant literature using search terms including ‘gastric satiety, intestine + satiety, satiation, cholecystokinin, ghrelin, peptide YY, glucagon-like peptide-1 and ileal brake’.

Results  Satiation, satiety and food intake result, among other factors, from signals originating in the stomach caused by distension and signals from the small intestine. These intestinal signals result from nutrient sensing in the gut and activate neural and humoral pathways. Activation of the distal part of the gut, the so called ileal brake, leads to reduction in hunger and food intake, and models of chronic ileal brake activation lead to massive weight loss.

Conclusion  Gastrointestinal signals are crucial for the regulation of food intake, satiety and satiation. The ileal brake deserves special attention, as both ileal intubation studies and surgical studies demonstrate that activation of the ileal brake reduces food intake. In the surgical models, weight loss occurs without adaptation to the anorectic effects of ileal brake activation.