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W2344909704 abstract "The fundamental gastrointestinal functions include motility, sensation, absorption, secretion, digestion, and intestinal barrier function. Digestion of food and absorption of nutrients normally occurs without conscious perception. Symptoms of functional gastrointestinal disorders often are triggered by meal intake, suggesting abnormalities in the physiological processes are involved in the generation of symptoms. In this article, normal physiology and pathophysiology of gastrointestinal function, and the processes underlying symptom generation, are critically reviewed. The functions of each anatomic region of the digestive tract are summarized. The pathophysiology of perception, motility, mucosal barrier, and secretion in functional gastrointestinal disorders as well as effects of food, meal intake, and microbiota on gastrointestinal motility and sensation are discussed. Genetic mechanisms associated with visceral pain and motor functions in health and functional gastrointestinal disorders are reviewed. Understanding the basis for digestive tract functions is essential to understand dysfunctions in functional gastrointestinal disorders. The fundamental gastrointestinal functions include motility, sensation, absorption, secretion, digestion, and intestinal barrier function. Digestion of food and absorption of nutrients normally occurs without conscious perception. Symptoms of functional gastrointestinal disorders often are triggered by meal intake, suggesting abnormalities in the physiological processes are involved in the generation of symptoms. In this article, normal physiology and pathophysiology of gastrointestinal function, and the processes underlying symptom generation, are critically reviewed. The functions of each anatomic region of the digestive tract are summarized. The pathophysiology of perception, motility, mucosal barrier, and secretion in functional gastrointestinal disorders as well as effects of food, meal intake, and microbiota on gastrointestinal motility and sensation are discussed. Genetic mechanisms associated with visceral pain and motor functions in health and functional gastrointestinal disorders are reviewed. Understanding the basis for digestive tract functions is essential to understand dysfunctions in functional gastrointestinal disorders. The complex process of digestion of food and absorption of nutrients normally occurs without conscious perception. Symptoms reported by patients with functional gastrointestinal disorders often are triggered by meal intake, suggesting that abnormalities in the physiological processes involved in digestion are involved. Evaluation of sensory function and gastrointestinal motility aims to identify abnormalities in neuromuscular function to ultimately guide therapeutic management. In this article, more general and region-specific aspects of normal physiology and pathophysiology, and the processes underlying symptom generation, are critically discussed. The fundamental gastrointestinal functions include sensation, motility, digestion, absorption, and secretion. Human beings have the capability to consciously perceive a variety of highly differentiated sensations originating from the upper and lower sections of the gut. In the upper gastrointestinal (GI) tract, specific sensations amenable to conscious awareness range from temperature, taste, hunger, fullness, satiety, nausea, and pain. In the small and large bowel, distensions and contractions cause aversive sensations such as nausea, bloating, cramping, discomfort, and pain. Only a minority of the sensory information arising from the gastrointestinal tract is perceived consciously. The majority (estimated to be >90%) of afferent sensory information from the viscera serves homeostatic functions. The gastrointestinal tract is densely innervated to provide information on its luminal contents, processes regulating digestion and absorption, and potential threats.1Brookes S.J. Spencer N.J. Costa M. et al.Extrinsic primary afferent signalling in the gut.Nat Rev Gastroenterol Hepatol. 2013; 10: 286-296Crossref PubMed Scopus (7) Google Scholar This information was collected by intrinsic and extrinsic afferent nerves and regulates physiological responses for homeostasis and health. In brief, sensory neurons of the enteric nervous system activate local responses. Extrinsic afferent nerves transmit sensory information to the spinal cord or brainstem for further processing and integration (for brain processing, see later). In general, the extrinsic afferent innervation of the gut is conducted through the vagus nerve and the spinal afferents. The cell bodies of the vagus afferents are in the nodose ganglion, and mainly project to the nucleus of the solitary tract. Vagovagal reflexes result in stimulation of vagal efferents in the dorsal motor nucleus of the vagus nerve. Two examples of vagovagal reflexes are transient lower esophageal sphincter relaxations and meal-induced gastric accommodation. The spinal afferents have cell bodies in dorsal root ganglia. These afferents are thoracolumbar (with neurons in thoracolumbar dorsal root ganglia and projections via splanchnic nerves and mesenteric/colonic/hypogastric nerves) or lumbosacral (with cell bodies in lumbosacral dorsal root ganglia and projections via pelvic nerves and rectal nerves to the distal bowel) nerves, which synapse in the spinal cord and send information to the brainstem. Of note, each region of the GI tract receives dual sensory innervation reflecting functional connectivity for the distribution of extrinsic primary afferents in these pathways. Elucidating the afferent and central mechanisms mediating the specific sensation of visceral hyperalgesia or pain is relevant in the context of the functional gastrointestinal disorders (FGIDs), especially irritable bowel syndrome (IBS) and functional dyspepsia.2Mayer E.A. Gut feelings: the emerging biology of gut-brain communication.Nat Rev Neurosci. 2011; 12: 453-466Crossref PubMed Scopus (212) Google Scholar, 3Van Oudenhove L. Aziz Q. The role of psychosocial factors and psychiatric disorders in functional dyspepsia.Nat Rev Gastroenterol Hepatol. 2013; 10: 158-167Crossref PubMed Scopus (34) Google Scholar The sensation of pain appears to be mediated by different afferents depending on the location of the GI tract undergoing the noxious stimulus. Pain from the rectum primarily involves pelvic pathways; more proximal intestinal sensations are mediated by thoracolumbar spinal afferents. Inflammation (or inflammatory mediators) can change both the response properties of specific classes of sensory neurons and the involvement of specific ascending pathways, which is relevant in postinflammatory hypersensitivity and postinfectious IBS.4Keszthelyi D. Troost F.J. Masclee A.A. Irritable bowel syndrome: methods, mechanisms, and pathophysiology. Methods to assess visceral hypersensitivity in irritable bowel syndrome.Am J Physiol Gastrointest Liver Physiol. 2012; 303: G141-G154Crossref PubMed Scopus (35) Google Scholar For the sensations of hunger, satiety, fullness, and nausea, which play a prominent role in functional gastroduodenal disorders, vagal afferent pathways play a primary role. Vagal mucosal afferent pathways are activated by enteroendocrine cell mediators including cholecystokinin, ghrelin, and glucagon-like peptide-1, which regulate food intake and satiety.1Brookes S.J. Spencer N.J. Costa M. et al.Extrinsic primary afferent signalling in the gut.Nat Rev Gastroenterol Hepatol. 2013; 10: 286-296Crossref PubMed Scopus (7) Google Scholar Ghrelin is released from gastric endocrine cells and inhibits intraganglionic laminar endings located in myenteric ganglia. Abdominal vagal afferents can contribute to nausea and vomiting, at least in part through effects of 5-hydroxytryptamine released by enterochromaffin cells.1Brookes S.J. Spencer N.J. Costa M. et al.Extrinsic primary afferent signalling in the gut.Nat Rev Gastroenterol Hepatol. 2013; 10: 286-296Crossref PubMed Scopus (7) Google Scholar Multiple or multimodal ascending and descending pathways are involved in gastrointestinal sensation through bottom-up and top-down connections between the central nervous system and the GI tract along the brain–gut axis. Within the brain, the multiple facets that define the conscious experience of pain or other sensations are shaped, involving sensory–discriminative as well as affective–motivational aspects, behavioral–motor responses, and cognitive components. Multiple brain regions and interconnected networks mediate normal and disturbed responses to visceral stimulation. From the spinal cord, nociceptive ascending signals from the gut reach the brain via the anterolateral and dorsal column pathways.5Wilder-Smith C.H. The balancing act: endogenous modulation of pain in functional gastrointestinal disorders.Gut. 2011; 60: 1589-1599Crossref PubMed Scopus (38) Google Scholar The spinothalamic tract projects to the ventral nuclei of the thalamus and the medial thalamus and then to the primary and secondary somatosensory cortices. These structures primarily mediate the sensory–discriminatory aspects of noxious stimulation, including information regarding intensity, duration, and location. Affective–motivational aspects of pain probably are shaped via connections between the medial thalamus and the limbic system, including the anterior cingulate cortex as well as the midbrain, including the periaqueductal gray. The spinoreticular and spinomesencephalic tracts are additional anterolateral afferent systems that conduct sensory information to various loci within the brainstem, mediating reflexive, affective, and motivational consequences of noxious stimulation. Other cortical and subcortical brain regions in normal and abnormal visceral stimulus processing include the insula, the dorsolateral and ventrolateral prefrontal cortices, and the amygdala. These regions play a role in modulation of the response to pain by emotions such as stress and cognitions such as expectations in healthy human beings, as well as in patients with chronic pain or hyperalgesia. Descending corticolimbic pain modulation via inhibitory pathways involving the brainstem modulates afferent visceral signaling. Disturbed endogenous pain modulation probably plays a role in abnormal brain responsiveness to visceral pain stimuli in FGIDs.6Elsenbruch S. Rosenberger C. Enck P. et al.Affective disturbances modulate the neural processing of visceral pain stimuli in irritable bowel syndrome: an fMRI study.Gut. 2010; 59: 489-495Crossref PubMed Scopus (93) Google Scholar, 7Tillisch K. Labus J.S. Advances in imaging the brain-gut axis: functional gastrointestinal disorders.Gastroenterology. 2011; 140: 407-411Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar The major functions of human digestive tract motility are to accomplish propulsion along the gut, to mix gut contents with digestive secretions and expose them to the absorptive surface, to facilitate temporary storage in certain regions of the gut, to prevent retrograde movement of contents from one region to another, and to dispose of residues. In each region of the gastrointestinal tract, the muscle layers of the gut wall and their innervation are adapted and organized to produce the specific motor patterns that serve the motor functions. The entire gastrointestinal tract interacts with the central nervous system and communication between various parts of the gut is facilitated by the longitudinal transmission of myogenic and neurogenic signals through the intrinsic neurons, as well as by reflex arcs through autonomic neurons. The aspects of gut motility that appear most relevant to the FGIDs are contractile activity and tone, compliance, and transit. Phasic (short-duration) contractions originate from electrical spikes on the plateau phase of the slow-wave activity, and thus the frequency of the phasic contractions in the stomach and small intestine is dictated by the slow wave frequency. The slow-wave frequency varies along the length of the gastrointestinal tract; the maximum contractile frequency varies similarly. The maximum contractile frequency in the stomach is approximately 3 per minute, whereas in the small intestine the frequency decreases gradually from approximately 12 per minute in the duodenum to 7 per minute in the terminal ileum. A mixture of slow-wave frequencies is found in the colon and ranges from 1 to 12 per minute where the correlation between electrical and contractile activities is less clear. Whether the gut phasic contractions accomplish mainly mixing or propulsion depends on their temporal (eg, frequency, duration) and spatial (eg, spread of propagation) characteristics.8Sarna S.K. Myoelectrical and contractile activities of the gastrointestinal tract.in: Schuster M.M. Crowell M.D. Koch K.L. Schuster atlas of gastrointestinal motility in health and disease. 2nd ed. BC Decker, Inc, Ontario2002: 1-18Google Scholar A more prolonged state of contraction, referred to as tone, is not regulated by slow waves and may be recognized clearly in the proximal stomach (accommodation response to a meal) and the colon (response to feeding), as well as in some sphincteric regions. Tone is regulated by actin–myosin interaction mediated by cellular mechanisms that are modulated by neurogenic and mechanical stimuli. Phasic contractions, such as those regulating lumen occlusion, may be superimposed on tonic activity. Thus, tone can increase the efficiency of phasic contractions by diminishing the diameter of the lumen. Tone also modifies wall tension in response to gut filling, and is therefore one determinant of perception of distension.9Notivol R. Coffin B. Azpiroz F. et al.Gastric tone determines the sensitivity of the stomach to distention.Gastroenterology. 1995; 108: 330-336Abstract Full Text PDF PubMed Scopus (144) Google Scholar, 10Distrutti E. Azpiroz F. Soldevilla A. et al.Gastric wall tension determines perception of gastric distention.Gastroenterology. 1999; 116: 1035-1042Abstract Full Text Full Text PDF PubMed Scopus (176) Google Scholar Compliance refers to the capability of a region of the gut to adapt to intraluminal distension, expressed as the ratio of the change in volume to the change in pressure. Several factors contribute to compliance including the capacity (diameter) of the organ, the elastic properties of the gut wall (ie, thickness, fibrotic component, muscular activity), and the elasticity of surrounding organs (which can be influenced by fibrosis, ascites, abdominal masses). Although compliance sometimes has been expressed as the pressure/volume ratio at one distension step, it is expressed more accurately as the entire pressure/volume curve. Compliance can differ markedly in different regions of the gut, and even within an organ; for example, the descending colon is less compliant than the ascending colon, whereas the sigmoid colon is less compliant than the transverse colon. Compliance decreases during contraction and increases during relaxation, and in a given organ is determined by the muscular activity of its walls. Hence, short-term changes in compliance reflect the tone of the organ. In that respect, compliance measurements in vivo (volume/pressure relationship) reflect the elongation/tension relationship of the gut wall. A distending intraluminal volume produces a stretch and tension (force) on the gut wall, which determines the intraluminal pressure increment. Perception of gut distension is in part determined by wall tension, rather than by intraluminal volume or pressure. Hence, assessment of wall tension may be important in assessing perception of visceral stimuli.10Distrutti E. Azpiroz F. Soldevilla A. et al.Gastric wall tension determines perception of gastric distention.Gastroenterology. 1999; 116: 1035-1042Abstract Full Text Full Text PDF PubMed Scopus (176) Google Scholar, 11Tack J. Bisschops R. Sarnelli G. Pathophysiology and treatment of functional dyspepsia.Gastroenterology. 2004; 127: 1239-1255Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar, 12Distrutti E. Salvioli B. Azpiroz F. et al.Rectal function and bowel habit in irritable bowel syndrome.Am J Gastroenterol. 2004; 99: 131-137Crossref PubMed Scopus (41) Google Scholar, 13Corsetti M. Cesana B. Bhoori S. et al.Rectal hyperreactivity to distention in patients with irritable bowel syndrome: role of distention rate.Clin Gastroenterol Hepatol. 2004; 2: 49-56Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar Although flow reflects the local movements of intraluminal content, transit refers to the time taken for food or other material to traverse a specified region of the gastrointestinal tract. Transit represents the net interaction of a number of parameters and is a relevant and convenient index of organ function. Most measurements of transit are based on detecting intraluminal movements of an extrinsic marker labeling the luminal content. Transit depends on many factors, such as the physical (eg, solid, liquid, gas) and chemical (eg, pH, osmolality, and nutrient composition) nature of both gut contents and the administered marker. Transit measurement also is influenced by the state of gut motility at the time of marker administration (eg, fasted vs fed motility), and any preparation of the gut (eg, cleansing of the colon). The transit times have been shown to be abnormal in some FGIDs. The relationship between transit and phasic activity or tone is incompletely understood, but studies examining the movement of radiolabeled colonic contents in healthy subjects have shown that only 28% are associated with propagating sequences, with the remainder associated with either nonpropagating activity (32%) or no pressure events (40%).14Cook I.J. Furukawa Y. Panagopoulos V. et al.Relationships between spatial patterns of colonic pressure and individual movements of content.Am J Physiol Gastrointest Liver Physiol. 2000; 278: G329-G341PubMed Google Scholar Moreover, patients with chronic constipation who have normal transit can show reduced fasting and/or postprandial colonic tone.15Ravi K. Bharucha A.E. Camilleri M. et al.Phenotypic variation of colonic motor functions in chronic constipation.Gastroenterology. 2010; 138: 89-97Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar Interest in the role of abnormal barrier function in FGIDs has increased since the observation that postinfectious IBS is associated with increased permeability and increased rectal mucosal enteroendocrine cells and T lymphocytes.16Camilleri M. Madsen K. Spiller R. et al.Intestinal barrier function in health and gastrointestinal disease.Neurogastroenterol Motil. 2012; 24: 503-512Crossref PubMed Scopus (110) Google Scholar A tightly regulated intestinal barrier is present to protect us against threats from the intestinal lumen.16Camilleri M. Madsen K. Spiller R. et al.Intestinal barrier function in health and gastrointestinal disease.Neurogastroenterol Motil. 2012; 24: 503-512Crossref PubMed Scopus (110) Google Scholar, 17Neunlist M. Van Landeghem L. Mahe M.M. et al.The digestive neuronal-glial-epithelial unit: a new actor in gut health and disease.Nat Rev Gastroenterol Hepatol. 2013; 10: 90-100Crossref PubMed Scopus (43) Google Scholar, 18Fasano A. Intestinal permeability and its regulation by zonulin: diagnostic and therapeutic implications.Clin Gastroenterol Hepatol. 2012; 10: 1096-1100Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar At first, gastric acid and pancreatic juice degrade bacteria and antigens in the lumen. Next, the enterocytes are covered by an unstirred water layer, the glycocalyx, and, finally, a mucus layer secreted by goblet cells providing some kind of physical barrier against intraluminal bacteria. Together with secreted factors such as defensins secreted by Paneth cells and secretory immunoglobulins released by enterocytes, a subtle equilibrium with the external milieu is created within this layer covering the epithelium (Figure 1). The epithelium is tightly sealed by 3 types of junctional complexes between the enterocytes: (1) tight junctions, (2) adherent junctions, and (3) desmosomes. Tight junctions are the most apical intercellular protein complex formed by transmembrane proteins such as claudins, occludin, and tricellulin, which are connected to the actin cytoskeleton via zona occludens. They are mainly responsible for the sealing of the intercellular space and regulate the passage of particles in a rather complicated manner with sometimes opposing functions.16Camilleri M. Madsen K. Spiller R. et al.Intestinal barrier function in health and gastrointestinal disease.Neurogastroenterol Motil. 2012; 24: 503-512Crossref PubMed Scopus (110) Google Scholar Interaction with the strength of the tight junctions will increase permeability to large solutes with no charge discrimination, a pathway referred to as the leak pathway. Adherent junctions are located below the tight junctions and are linked to the actin cytoskeleton through multiprotein complexes consisting of the transmembrane protein E-cadherin and the intracellularly localized catenins.17Neunlist M. Van Landeghem L. Mahe M.M. et al.The digestive neuronal-glial-epithelial unit: a new actor in gut health and disease.Nat Rev Gastroenterol Hepatol. 2013; 10: 90-100Crossref PubMed Scopus (43) Google Scholar Together with desmosomes, the third type of junctional complexes located at the basal pole of the intercellular space, they comprise strong adhesive bonds between epithelial cells, providing mechanical strength to the epithelial barrier. Stimuli modulating the strength of these bonds also thus will contribute to a more leaky barrier. Mainly from animal work, several factors have been proposed, such as genetic predisposition, alterations in the microbiome (including bacterial infection), and psychological stress (through mast cell activation). In human beings, the evidence is limited. Patients carrying a single-nucleotide polymorphism in the gene encoding for cadherin-1, one of the proteins of the adherent junctions, are at higher risk of developing postinfectious IBS.19Villani A.C. Lemire M. Thabane M. et al.Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis.Gastroenterology. 2010; 138: 1502-1513Abstract Full Text Full Text PDF PubMed Scopus (124) Google Scholar Glutamine synthase, a key enzyme in the synthesis of glutamine, is reduced in the intestinal mucosa of diarrhea-predominant IBS patients with increased permeability.20Zhou Q. Souba W.W. Croce C.M. et al.MicroRNA-29a regulates intestinal membrane permeability in patients with irritable bowel syndrome.Gut. 2010; 59: 775-784Crossref PubMed Scopus (86) Google Scholar Glutamine is a major energy source for rapidly dividing mucosal cells such as enterocytes, and thus important for the maintenance of intestinal barrier function. In human beings, cold pain stress and psychological stress result in increased levels of mast cell mediators in jejunal fluid,21Guilarte M. Santos J. de Torres I. et al.Diarrhoea-predominant IBS patients show mast cell activation and hyperplasia in the jejunum.Gut. 2007; 56: 203-209Crossref PubMed Scopus (209) Google Scholar, 22Santos J. Saperas E. Nogueiras C. et al.Release of mast cell mediators into the jejunum by cold pain stress in humans.Gastroenterology. 1998; 114: 640-648Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar whereas psychological stress and infusion of corticotropin-releasing hormone induce increased permeability in healthy subjects. Mast cell activation induced by stress may be one of the mechanisms leading to barrier dysfunction in human beings (Figure 2). Increased proteolytic activity in the intestinal lumen,23Roka R. Rosztoczy A. Leveque M. et al.A pilot study of fecal serine-protease activity: a pathophysiologic factor in diarrhea-predominant irritable bowel syndrome.Clin Gastroenterol Hepatol. 2007; 5: 550-555Abstract Full Text Full Text PDF PubMed Scopus (70) Google Scholar, 24Gecse K. Roka R. Ferrier L. et al.Increased faecal serine protease activity in diarrhoeic IBS patients: a colonic lumenal factor impairing colonic permeability and sensitivity.Gut. 2008; 57: 591-599Crossref PubMed Scopus (155) Google Scholar caused by either pancreatic enzymes or bacterial proteases, can lead to barrier dysfunction.24Gecse K. Roka R. Ferrier L. et al.Increased faecal serine protease activity in diarrhoeic IBS patients: a colonic lumenal factor impairing colonic permeability and sensitivity.Gut. 2008; 57: 591-599Crossref PubMed Scopus (155) Google Scholar Application of diarrhea-predominant IBS fecal supernatant on colonic mucosa results in a rapid increase in phosphorylation of myosin light chain and delayed redistribution of zonula occludens-1 in colonocytes. Although abnormalities in secretion have not been studied in depth in FGIDs, interest in mechanisms triggering secretion has increased tremendously since the observation that compounds activating secretion are efficacious as treatment for functional constipation and constipation-predominant IBS.25Lembo A.J. Kurtz C.B. Macdougall J.E. et al.Efficacy of linaclotide for patients with chronic constipation.Gastroenterology. 2010; 138: 886-895Abstract Full Text Full Text PDF PubMed Scopus (113) Google Scholar Linaclotide, a 14–amino acid peptide homologous to bacterial heat-stable enterotoxins, activates receptor guanylyl cyclase C in the brush border of intestinal mucosa cells from the duodenum to rectum to open the cystic fibrosis transmembrane conductance regulator chloride channel, producing a net efflux of ions and water into the intestinal lumen.26Bharucha A.E. Waldman S.A. Taking a lesson from microbial diarrheagenesis in the management of chronic constipation.Gastroenterology. 2010; 138: 813-817Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar Lubiprostone, an activator of chloride channels, is a member of a class of compounds called prostones,27Norimatsu Y. Moran A.R. MacDonald K.D. Lubiprostone activates CFTR, but not ClC-2, via the prostaglandin receptor (EP(4)).Biochem Biophys Res Commun. 2012; 426: 374-379Crossref PubMed Scopus (14) Google Scholar and results in increased chloride secretion with associated passive transport of sodium and water across the epithelium, thereby enhancing fluid secretion. Bile acids potently induce secretion and colonic motility.28Shin A. Camilleri M. Vijayvargiya P. et al.Bowel functions, fecal unconjugated primary and secondary bile acids, and colonic transit in patients with irritable bowel syndrome.Clin Gastroenterol Hepatol. 2013; 11: 1270-1275Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar Increased exposure of the colonic mucosa owing to reduced reabsorption in the distal small intestine (bile acid malabsorption) has been implicated in a subgroup of patients with diarrhea-predominant IBS.29Wong B.S. Camilleri M. Carlson P. et al.Increased bile acid biosynthesis is associated with irritable bowel syndrome with diarrhea.Clin Gastroenterol Hepatol. 2012; 10: 1009-1015 e3Abstract Full Text Full Text PDF PubMed Scopus (49) Google Scholar Conversely, patients with constipation-predominant IBS or functional constipation have impaired bile acid synthesis,30Abrahamsson H. Ostlund-Lindqvist A.M. Nilsson R. et al.Altered bile acid metabolism in patients with constipation-predominant irritable bowel syndrome and functional constipation.Scand J Gastroenterol. 2008; 43: 1483-1488Crossref PubMed Scopus (23) Google Scholar indicating that alterations in bile acid metabolism may be implicated in the pathophysiology of functional gastrointestinal disorders. In the context of the FGIDs, gastrointestinal dysmotility can develop through several mechanisms involving the brain–gut axis. First, various inflammatory, immune, infiltrative, or degenerative processes may directly affect the muscle and/or other elements of the enteric nervous system effector system. Dysmotility also may be triggered indirectly in response to excess stimulation by visceral afferent (sensory) fibers that influence local gastrointestinal motor function via modulation of motor neurons in prevertebral ganglia. In addition, activation of visceral afferent fibers induces autonomic changes integrated in the brainstem, such as changes in heart rate, and alterations in colonic tone (eg, vagally mediated gastrocolonic motor response), which may be increased in certain FGIDs. Finally, psychosocial stressors can induce mast cell activation affecting motility, mucosal permeability, and visceral afferents (Figure 2). The meal ingested is transformed from the mouth to the ileum, first by digestion and then by absorption, so that only nonabsorbed residues pass into the colon. The whole digestive–absorptive process down to the terminal ileum is finely regulated depending on the composition of intraluminal content; nutrients in the stomach and small bowel have limited effects on colonic activity. Nonabsorbed meal residues entering the colon serve as substrate to feed microbiota and this interaction has several effects, including the modulation of the digestive system. During fasting, the gastrointestinal tract exerts cyclic activity with alternating periods of quiescence and periods of intense motor and secretory activity (Figure 3). This stereotyped pattern develops in the absence of extrinsic stimuli and its function seems to be the clearance of residues from the gut lumen. Ingestion of a meal stimulates the digestive system, suppresses the intrinsic interdigestive pattern, and activates reflexes that control the digestive process. The presence of nutrients in the gastrointestinal tract modulates gastrointestinal motility, barrier function (secretion, absorption), as well as sensitivity. Even before ingestion, the digestive system" @default.
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W2344909704 title "Fundamentals of Neurogastroenterology: Physiology/Motility – Sensation" @default.
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