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Neuroendocrine tumours
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Sairah R Khan, Kathryn L Wallitt, Adil Al-Nahhas, Tara D Barwick
Duodenal NETs are clinically and pathologically distinct from other small bowel NETs. They rarely arise from enterochromaffin cells, so serotonin excess and classic carcinoid syndrome is rarely seen (5). They arise from either gastrin-producing G cells (duodenal gastrinomas) or somatostatin-producing D cells (duodenal somatostatinomas). Duodenal somatostatinomas are typically periampullary with an association with NF1 in up to 50% of cases (109). Duodenal gastrinomas are either sporadic or associated with MEN1, in which case they are often multiple (16).
The Small IntestineSecretions, Digestion and Motility
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Intestinal epithelial transport is regulated by neurotransmitters released by the enteric nervous system. Acetylcholine and vasoactive intestinal peptide stimulate epithelial cells the secrete Cl− ions. This inhibits NaCl absorption. The local passage of food promotes the release of serotonin from enterochromaffin cells. This stimulates Cl− secretion and thus fluid secretion. Local production of prostaglandins in the intestine plays an important role in stimulating Cl− and secretion. Aldosterone has a role in water and electrolyte reabsorption in chronic (over days to weeks) situations. With a low salt diet, aldosterone is released and increases Na+ transporters required for Na+ absorption in the colon.
Serotonin as an Intestinal Secretagogue
Published in T.S. Gaginella, J.J. Galligan, SEROTONIN and GASTROINTESTINAL FUNCTION, 2020
The major source of intestinal 5-HT is the enterochromaffin cells. Small amounts of 5-HT are found in myenteric neurons and in mucosal mast cells, where it is probably stored together with histamine.5 The 5-HT-containing enterochromaffin cells represent the largest subpopulation of endocrine cells in the human intestinal wall, with their frequency decreasing from proximal to distal segments of the gut.6,7 In the rat, the largest amount of gastrointestinal 5-HT is located in the cecum.8 In the rabbit duodenum, the 5-HT content is 9.4 ± 0.6 μg per gram wet weight, only 0.38% of which is present in the longitudinal and circular muscle layers that contain the myenteric nerve plexus and most of the submucous nerve plexus.9 A similar distribution was found in the guinea pig, proving that the vast majority of the 5-HT in the gut is present in the mucosa.10 In rats and mice, substantial amounts of 5-HT are also present in mucosal and connective tissue mast cells,5,11 which show some differences to each other in their mediator content and their degranulation response to pharmacologic agents.12 Less information is available about mast cell heterogeneity in humans. Symptoms of intestinal fluid loss have been associated with mast cell degranulation, releasing histamine,13 leukotrienes,14 and 5-HT.15
Gut microbiota-motility interregulation: insights from in vivo, ex vivo and in silico studies
Published in Gut Microbes, 2022
Barbora Waclawiková, Agnese Codutti, Karen Alim, Sahar El Aidy
It is well accepted that the greatest quantity of serotonin (5-HT) in the human body is synthesized within a subtype of the enteroendocrine cells, enterochromaffin cells, in the intestinal mucosa, via the enzyme tryptophan hydroxylase 1 (TPH1).78 Enterochromaffin cells act as sensory transducers to release 5-HT in response to various mechanical and chemical stimuli.79 In 2017, enterochromaffin cells were recognized as specialized stimulus detectors that constitute a direct line of communication between the mouse gut epithelium and enteric nervous system.80 A year later, it was shown that, throughout the mouse gut, enterochromaffin cells release 5-HT in response to their sensing of nutrients and microbial metabolites, indirectly through the release of GLP-1 by neighboring cells.81
Microbiota-derived metabolites as drivers of gut–brain communication
Published in Gut Microbes, 2022
Hany Ahmed, Quentin Leyrolle, Ville Koistinen, Olli Kärkkäinen, Sophie Layé, Nathalie Delzenne, Kati Hanhineva
Other forms of indirect enteric neuron activation are the enteroendocrine signaling by colonic L cells or enterochromaffin cells. The colonic enterochromaffin cells produce the majority of the circulating serotonin in the human blood.189 As discussed previously, several bacterial metabolites have been shown to influence the enterochromaffin cells’ serotonin synthesis.9 Enteric neurons in the submucosa are in close proximity of the translocated serotonin from the lumen and express serotonin receptors. In addition to neuronal stimulation, serotonin might have a role in the development, maturation, and protection of the enteric nervous system.190 Similar to enterochromaffin cells, colonic L cells are activated by microbial metabolites, such as SCFAs and secondary bile acids among others.188 The L cells produce bioactive peptides such as GLP-1 and PYY both known for their local effects on gut motility and secretion, and central effects on food intake and feeding behavior.191–193 The hormones released by L cells have multiple effectors, including enteric neurons and vagus nerve, that carry the signal toward CNS.194 However, recently Bohórquez et al.195 uncovered a neuroepithelial circuit connecting the enteroendocrine cell to sensory neurons, together referred as neuropods. This suggests that among the endocrine signaling, the enteroendocrine cells could form physical connections with the neurons as a conduit for sensory transmission activated by microbial metabolites.
Effect of wheat bran derived prebiotic supplementation on gastrointestinal transit, gut microbiota, and metabolic health: a randomized controlled trial in healthy adults with a slow gut transit
Published in Gut Microbes, 2020
Mattea Müller, Gerben D. A. Hermes, Canfora Emanuel E., Jens J. Holst, Erwin G. Zoetendal, Hauke Smidt, Freddy Troost, Frank G. Schaap, Steven Olde Damink, Johan W. E. Jocken, Kaatje Lenaerts, Ad A. M. Masclee, Ellen E. Blaak
Colonic SCFA may affect gastrointestinal motility via stimulation of enterochromaffin cells amongst other mechanisms.58 Despite the increase of acetate-producing Bifidobacterium, plasma and fecal SCFA concentrations were not affected by AXOS intervention. Of note, we observed a time-dependent decrease in plasma acetate and butyrate in both groups reflecting a high temporal variability in SCFA metabolism. Circulating acetate and butyrate have several sources: 1) direct exogenous ingestion via food sources, 2) indirect exogenous production by colonic bacterial fermentation of non-digested food components, and 3) endogenous production from protein, lipid, and carbohydrate catabolism in mainly the liver.4 Plasma SCFA concentrations are thus the net result of SCFA production, absorption and splanchnic extraction/hepatic metabolism, and are therefore difficult to interpret. Since rate of appearance from endogenous or exogenous sources can only be acquired by using stable isotope tracer techniques, we cannot provide this information for the present study.