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The Nutrition-Focused History and Physical Examination (NFPE) in Malnutrition
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Secretin also stimulates hepatic bile production. The gallbladder is then stimulated to contract by duodenal cholecystokinin release from enteroendocrine I cells. This sends bile into the duodenum to emulsify dietary fat and enable pancreatic lipase to act upon it. As digestion occurs, the food bolus is degraded and nutrients are absorbed. Peristalsis pushes the food bolus down the bowel until it reaches the ileocecal valve. When the valve opens, the undigested remnants (also called the residual) move into the cecum and start to process into stool. Gut bacteria act on some of this residual to produce short chain fatty acids. The remainder, along with sloughed luminal cells and bacteria, are passed out the rectum.
Physiological and Pathophysiological Roles of VIP, Somatostatin, Opioids, Galanin, GRP, and Secretin
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Jan D. Huizinga, Julio Pintin-Quezada
Secretin is a 27-amino-acid peptide. Secretin belongs to the same “peptide family” as VIP. Secretin is released from endocrine cells in the small intestine. Secretin stimulates pancreatic secretion and bile flow, but it inhibits gastric acid secretion.
Endocrine System
Published in David Sturgeon, Introduction to Anatomy and Physiology for Healthcare Students, 2018
The stomach also produces the peptide hormone gastrin in response to distension of the pyloric antrum (see Chapter 11, Figure 11.3). Gastrin stimulates the production of hydrochloric acid and intrinsic factor (necessary for the absorption of vitamin B12) by the parietal cells of the gastric mucosa. It is also responsible for the secretion of pepsinogen (the inactive precursor of the enzyme pepsin) by the chief cells of the stomach and encourages contraction of gastric smooth muscle to aid digestion. We also noted in Chapter 11, that the small intestine produces the peptide hormones cholecystokinin (CCK) and secretin. CCK derives its name from the Greek for ‘bile + sac + move’ (chole + cysto + kinin) and it stimulates the contraction of the gall bladder and the expulsion of bile. It also increases the production of digestive enzymes by the acinar cells of the pancreas and relaxes the hepatopancreatic sphincter which allows pancreatic juice and bile to enter the duodenum. Secretin, on the other hand, stimulates cells in the liver and pancreas to secrete alkaline bicarbonate into the duodenum that helps to neutralise the potentially damaging effects of acidic chyme on the epithelial cells and brush border of the small intestine. It also inhibits gastric motility and the production of gastric secretions.
High prevalence of gastrointestinal symptoms in patients with primary Sjögren’s syndrome cannot be attributed to pancreatic exocrine insufficiency
Published in Scandinavian Journal of Gastroenterology, 2022
Aleksandra Hedström, Marika Kvarnström, Greger Lindberg, Sandra Alsabeah, Hanna Alsabeah, Nelson Ndegwa, J. Matthias Löhr, Stephan L. Haas, Miroslav Vujasinovic
Gobelet et al. diagnosed PEI by using the N-benzoyl-L-Tyrosyl para-amino-benzoic acid test (NBT PABA test) and by measuring the trypsinemia by radioimmunoassay (RIA) in SS in comparison with normal controls. The NBT PABA test was pathological in 37.5% of SS but in none of the controls, and PEI was clinically silent. The RIA trypsinemia was found to be high in 6.2% of SS [9]. In a similar study by Coll et al. PEI was found in 63% of patients [10]. When comparing different quantitative pancreatic function tests, the NBT PABA was found to be ambiguous and unreliable, which resulted in this test being completely omitted from recent guidelines [5,32]. The measurement of trypsin in serum, like amylase, lipase, or even elastase, can be interpreted as a certain degree of (subclinical) inflammation within the putative pancreatic affection in SS. However, it cannot be used as a measurement of pancreatic exocrine function [33]. The pancreozymin-secretin test was used in a study by Hradský in 20 patients with SS, and showed disturbed pancreatic function with a diminished volume of pancreatic secretion and reduced output of bicarbonates after secretin injection [11]. Afzelius et al. examined the morphology, exocrine, and endocrine functions of the pancreas in SS using secretin-stimulated magnetic resonance cholangiopancreatography (sMRCP), a Lundh test, oral glucose tolerance test, and blood sampling. The rate of pancreatic dysfunction was 25–33% according to this study cohort [8].
The impact of ellagic acid on some apoptotic gene expressions: a new perspective for the regulation of pancreatic Nrf-2/NF-κB and Akt/VEGF signaling in CCl4-induced pancreas damage in rats
Published in Immunopharmacology and Immunotoxicology, 2021
Abdullah Aslan, Seda Beyaz, Ozlem Gok, Muhammed Ismail Can, Fazilet Erman, Orhan Erman
The pancreas is known as an internal (endocrine) and external (exocrine) secretory organ that it produces digestive enzymes, hormones and its weight is nearly 60–160 g in human. The pancreatic enzymes are stored and released by the cells of the exocrine section. Endocrine secretions are controlled by islets of Langerhans. Pancreatic secretion is controlled by secretin and cholecystokinin hormones produced by enteroendocrine cells in the duodenal mucosa. In addition to hormonal effect, autonomic innervation of the pancreas is also important in secretion. While the sympathetic nerve fibers regulate the blood flow of the pancreas, parasympathetic fibers are responsible for stimulating the activity of centroacinar cells and acinus [1]. Carbon tetrachloride (CCl4) is a powerful carcinogenic factor that causes the manufacture of initiates cell injury and reactive free radicals. It has been demonstrated to be a pulmonic toxic composite that leads degeneration of the alveolar septa with numerous deposition of fibroblasts, macrophages, and neutrophils in blood vessels and also liver is the primary organ involved in CCl4 intoxication [2,3]. In addition, it is a powerful hepatotoxic factor mostly used to crate liver damage in vivo by oxidative stress [4]. However, besides the liver, kidney, brain, lung, testis, and muscles have been also found to cause oxidative damage. CCl4 causes oxidative stress through causes tissue injury and free radical formation [5–7]. Under normal conditions, external stress and many internal factors always change cellular levels.
Preclinical insights into cholangiopathies: disease modeling and emerging therapeutic targets
Published in Expert Opinion on Therapeutic Targets, 2019
Keisaku Sato, Shannon Glaser, Lindsey Kennedy, Suthat Liangpunsakul, Fanyin Meng, Heather Francis, Gianfranco Alpini
Secretin (Sct) is a hormone that binds to secretin receptor (SR) thereby regulating cholangiocyte proliferation during cholestatic liver diseases [89,90]. SR is expressed in the basolateral domain of cholangiocytes in the liver, and the Sct/SR axis plays a critical role in the pathophysiology of cholangiopathies [91]. A recent study using Sct-/-, SR-/-, and Sct-/-SR-/- transgenic mice has demonstrated that these knockout mice have attenuated ductular reaction and liver fibrosis compared to wild-type during BDL-induced liver injury resulting from decreased secretion of TGF-β1 from cholangiocytes [92]. Another study has generated Mdr2-/-SR-/- mice and has demonstrated that these mice have improved liver pathology and reduced fibrosis compared to Mdr2-/- mice [93]. Knockout of SR decreased cellular senescence and secretion of SASP markers from cholangiocytes, such as CCL2 [93]. Administration of an SR antagonist, Sec 5-27, ameliorated ductular reaction and liver fibrosis in Mdr2-/- mice and BDL mice in vivo [94]. In PBC; however, functional roles of Sct may differ from those in PSC. A preliminary study has demonstrated that administration of Sct improves liver conditions by helping cholangiocyte functions in dnTGFβRII mice although effects of Sct may differ between early stage and late stage of PBC, and further studies are needed [95]. These studies suggest that inhibition or activation of the Sct/SR axis using inhibitors or agonists could be a novel therapeutic tool for PSC or PBC, respectively.