ReviewDigestive diseases and sciences2012
Enteroendocrine and neuronal mechanisms in pathophysiology of acute infectious diarrhea.
Review in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Racecadotril in the management of diarrhea: an underestimated therapeutic option?Therapeutic advances in gastroenterology · 2025Review
- Bioactivity-guided isolation of potential antidiarrheal constituents fromFrontiers in veterinary science · 2024Article
- Impact of Probiotics on the Prevention and Treatment of Gastrointestinal Diseases in the Pediatric Population.International journal of molecular sciences · 2023Review
- Garcinia buchananii stem bark extract and its bioactive constituents manniflavanone, GB-2 and buchananiflavanone attenuate intestinal inhibitory neuromuscular transmission.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2023Article
- Article
- Alterations in the Gut Microbiota and Metabolomics of Seafarers after a Six-Month Sea Voyage.Microbiology spectrum · 2022Article
- The α isoform of cGMP-dependent protein kinase 1 (PKG1α) is expressed and functionally important in intrinsic primary afferent neurons of the guinea pig enteric nervous system.Neurogastroenterology and motility · 2021Article
- Cholera and Pancreatic Cholera: Is VIP the Common Pathophysiologic Factor?Tropical medicine and infectious disease · 2020Article
- Travelers' Diarrhea: A Clinical Review.Recent patents on inflammation & allergy drug discovery · 2019Review
- Bacterial Signaling to the Nervous System through Toxins and Metabolites.Journal of molecular biology · 2017Review
- Microbiota and host determinants of behavioural phenotype in maternally separated mice.Nature communications · 2015Article
- Complex interactions among diet, gastrointestinal transit, and gut microbiota in humanized mice.Gastroenterology · 2013Article
- The immunopathogenesis of celiac disease reveals possible therapies beyond the gluten-free diet.Seminars in immunopathology · 2012Review
- Guanylate cyclase C signaling: an intestinal secretory pathway where bugs, genes and new drugs intersect.Genome medicine · 2012Article
- Translational approaches for pharmacotherapy development for acute diarrhea.Gastroenterology · 2012Article
Corrections and comments
- Commented on by
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWhile enterocyte secretion is the predominant mechanism considered responsible for secretory diarrhea in response to acute enteric infections, there are several lines of evidence that support alternative mechanisms controlling fluid and electrolyte secretion in diarrhea.
aimTo review enteroendocrine and neuronal mechanisms that participate in the development of acute infectious diarrhea. RECENT ADVANCES: Acute infectious diarrheas due to bacterial toxins (e.g., cholera, E. coli heat-stable enterotoxin, C. difficile) and rotavirus are all associated with secretion of transmitters from enteroendocrine cells (e.g., 5-HT) and activation of afferent neurons that stimulate submucosal secretomotor neurons. The latter secrete acetylcholine (which binds to muscarinic receptors on epithelial cells) and VIP. Involvement of nerves was demonstrated by inhibition of bacterial toxin-induced secretion by hexamethonium (nicotinic), tetrodotoxin (Na(+) channel blocker), and lidocaine (visceral/mucosal afferents). Nicotinic receptors are present on secretomotoneurons and these are activated by release of acetylcholine from enteric interneurons or extrinsic efferent fibers. Specific organisms also modify other mechanisms that may contribute to development of acute diarrhea. Thus, mucin secretion, activation of motor mechanisms, increased mucosal permeability and inhibition of bile acid absorption have been reported in specific types of acute infectious diarrhea.
conclusionNew therapies targeting neural and transmitter mediation including 5-HT, VIP, NPY, as well as toxin receptors and channels activated during acute infectious diarrhea could usher in a novel approach to enhancing glucose-electrolyte solutions used in the treatment of acute diarrhea.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.