J Maljaars1, H P F Peters, A M Masclee. 1. Division of Gastroenterology-Hepatology, Department of Internal Medicine, University Hospital Maastricht, Maastricht, The Netherlands. pwj.maljaars@intmed.unimaas.nl
Abstract
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.
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.
Authors: Vishal Ratanpaul; Dagong Zhang; Barbara A Williams; Simon Diffey; John L Black; Michael J Gidley Journal: Eur J Nutr Date: 2021-05-05 Impact factor: 5.614