China
Africa
Explore chapters and articles related to this topic
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
Enteroglucagons are peptides synthesised by the L cells in the intestine. The most important peptide is glucagon-like peptide-1 (GLP-1). It is a 39-amino-acid peptide that inhibits gastric secretion and emptying and enhances the secretion of insulin (making it an incretin). It is released in response to luminal sugars. Its physiological significance is not known.
The Identification of Cell Types in the Normal Adult Colon
Published in Leonard H. Augenlicht, Cell and Molecular Biology of Colon Cancer, 2019
As in other parts of the gastrointestinal tract, the colonic endocrine cells may synthesize and store more than one hormone or more than one form of a single hormone in the same cell. The enteroglucagon cell illustrates the existence of both of these phenomena in the adult colon. The enteroglucagon cells were originally defined ultrastructurally as both Alike cells due to their resemblance to the pancreatic A cells, and also as “L” cells due to their large SG averaging 300 to 400 nm.110-112 Subsequent parallel immunocytochemical and ultrastructural studies localized enteroglucagon to the “L” cell.113 More recently, both glicentin (a 100-amino acid gut type glucagon) and pancreatic type glucagon (a 29-amino acid sequence) have been localized within the same cell in the human colon,114 perhaps reflecting a precursor-product relationship. Alternatively, the colocalization of glicentin and peptide YY in the same colonic endocrine cells115 likely reflects the presence of two separate precursor molecules in the same cell, since PYY is not contained in the glicentin precursor.116
Stomach and duodenum
Published in Michael Gaunt, Tjun Tang, Stewart Walsh, General Surgery Outpatient Decisions, 2018
Symptoms of sweating and tremor due to hypoglycaemia occur 2–3 hours after a meal. Diagnosis is made by performing an in-patient extended glucose tolerance test. Following a meal this shows initial hyperglycaemia, provoking an exaggerated insulin release with increased plasma insulin and enteroglucagon levels. This results in the subsequent hypoglycaemia and occurrence of symptoms. Treatment is mainly dietary, with low carbohydrate-high protein meals. Ingesting fluids at the same time as solids should be avoided, to help reduce intestinal transit time.
Nutritional interventions and outcomes of children with short bowel syndrome in a tertiary hospital setting in South Africa
Published in South African Journal of Clinical Nutrition, 2023
BD Saayman, AJW Millar, E van Niekerk
Enteral feeding, either orally or via nasogastric tube, should be initiated as soon as possible after bowel resection, once the postoperative ileus has resolved, as it is seen to be the primary treatment of SBS. The type and timing of feed will be influenced by the residual bowel length and function, type of stoma, presence of ICV and colon. The presence of nutrients in the intestine is essential in promoting gut adaptation as adaptation is driven by the increased load of fatty acids, carbohydrates and proteins on the enteroglucagon-producing cells found in the ileum.9 The goal of feeding is to reduce the incidence of parenteral nutrition associated cholestasis (PNAC), decreasing diarrhoea and steatorrhea and dehydration, improving intestinal adaptation and reducing sepsis episodes.3,7,15
Changes in colonic enteroendocrine cells of patients with irritable bowel syndrome following fecal microbiota transplantation
Published in Scandinavian Journal of Gastroenterology, 2022
Tarek Mazzawi, Trygve Hausken, Magdy El-Salhy
Patients with IBS have altered densities of enteroendocrine cells throughout the GI tract [10,24–27] that tend to change following manipulations of diet [7,11,28–32] and of the gut microbiota [20,21]. Previous publication shows that dietary manipulation also affects the gut microbiota [33]. The dynamic changes that occur to the enteroendocrine cells following their interactions with the surrounding stimuli stimulate their release of the gut hormones to regulate the different functions of the GI tract [5,34]. Chromogranin A is a common marker for the enteroendocrine cells [35–38]. Serotonin modulates the GI visceral sensitivity [24,39–42] stimulates large intestinal motility, and accelerates intestinal transit time [39–47]. Somatostatin inhibits intestinal contraction [34,48], and stimulates the absorption of water and electrolytes [34]. PYY stimulates the absorption of water and electrolytes and is a major regulator of the ‘ileal brake’ [24,49]. Enteroglucagon (oxyntomodulin) inhibits gastric and pancreatic secretions and reduces gastric motility [48]. Pancreatic polypeptide inhibits pancreatic secretion; relaxes gall bladder; and stimulates motility of stomach and small intestine [48].