The gastrointestinal tract in hunger and satiety signalling

Abstract

Background: Different peripheral pathways are implicated in the regulation of the food ingestion-digestion cycle.Methods: Narrative review on gastrointestinal mechanisms involved in satiety and hunger signalling.Results: Combined mechano-and chemoreceptors, peripherally released peptide hormones and neural pathways provide feedback to the brain to determine sensations of hunger (increase energy intake) or satiation (cessation of energy intake) and regulate the human metabolism. The gastric accommodation reflex, which consists of a transient relaxation of the proximal stomach during food intake, has been identified as a major determinant of meal volume, through activation of tension-sensitive gastric mechanoreceptors. Motilin, whose release is the trigger of gastric Phase 3, has been identified as the major determinant of return of hunger after a meal. In addition, the release of several peptide hormones such as glucagonlike peptide 1 (GLP-1), cholecystokinin as well as motilin and ghrelin contributes to gut-brain signalling with relevance to control of hunger and satiety. A number of nutrients, such as bitter tastants, as well as pharmacological agents, such as endocannabinoid receptor antagonists and GLP-1 analogues act on these pathways to influence hunger, satiation and food intake. Conclusion:Gastrointestinal mechanisms such as gastric accommodation and motilin release are key determinants of satiety and hunger.

Mechanisms Underlying Food-Triggered Symptoms in Disorders of Gut-Brain Interactions

“…In FD, increased sensitivity to capsaicin administration has been reported, suggesting hypersensitivity to TRPV1 receptor activation ( 18 ). In healthy subjects, bitter tastants inhibit the release of motilin and ghrelin and suppress the occurrence of gastric phase 3, which is associated with decreased hunger sensations ( 19 , 20 ), but alterations in DGBI have not been studied to date. Low- or non-caloric sweeteners such as erythritol and xylitol do not alter plasma glucose or insulin levels, can stimulate the secretion of gut peptides such as CCK, GLP-1 and PYY, and slow down gastric emptying ( 21 , 22 ).…”

Nitric Oxide: From Gastric Motility to Gastric Dysmotility

“…This process of active relaxation is mediated by different parasympathetic reflex pathways, which lead to an increased NO release in humans [ 62 ]. Even if accommodation is usually considered as a mechanism which allows the stomach to prevent a rise in intragastric pressure during food intake [ 63 ], studies in humans have reported that ingestion of nutrients evokes an initial drop in the intragastric pressure, followed by a gradual recovery [ 64 ]. Gastric accommodation is based on fundal relaxation and studies in humans have shown such relaxation to be dependent upon NO [ 65 , 66 ].…”

“…The latter triggers stretch and tension, so stimulating mechanosensitive receptors which, in turn, communicate their information through the activation of the vagal afferent nervous fibers. These latter send signals to the hypothalamic regions involved in the regulation of food intake, through the interposition of the nucleus of the tractus solitarius [ 63 ]. Thus, besides anorexigenic gut hormones, such as cholecystokinin and glucagon-like peptide-1, which cause gastric distension and slow down emptying, satiety induced by gastric distension can also be regulated by some adipocyte-released peptides [ 63 , 73 ].…”

“…These latter send signals to the hypothalamic regions involved in the regulation of food intake, through the interposition of the nucleus of the tractus solitarius [ 63 ]. Thus, besides anorexigenic gut hormones, such as cholecystokinin and glucagon-like peptide-1, which cause gastric distension and slow down emptying, satiety induced by gastric distension can also be regulated by some adipocyte-released peptides [ 63 , 73 ]. So, NO being the major responsible for gastric relaxation might also have a role in the peripheral regulation of the hunger-satiety cycle.…”

Guidelines, top‐notch science & social media—Jump on the bandwagon

“…A reflection of this is the increasing followers' number of the UEG Journal Twitter account, reaching almost 6000 over barely 3 years. In 2021, we put emphasis on visual graphic content presentation in SoMe, as a distinction for 29 manuscripts published in UEG journal, covering the various GI fields including inflammatory bowel diseases, 12,13 endoscopy, 14 pancreas, 15,16 obesity, 17 gut, 18 GI tract physiology, 19 and the European guidelines. 1,2 We believe that an eye-friendly summary presentation form of published papers will beef up the UEG Journal overview and amplify the authors' effort.…”