ArticleDigestive diseases and sciences2009
Lubiprostone stimulates duodenal bicarbonate secretion in rats.
Article in Digestive diseases and sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 31 citations in OpenAlex.
- Evaluation of post-market adverse events of lubiprostone: a real-world adverse event analysis from the FAERS database.BMC gastroenterology · 2025Article
- The ClC-2 Chloride Channel Activator, Lubiprostone, Improves Intestinal Barrier Function in Biopsies from Crohn's Disease but Not Ulcerative Colitis Patients.Pharmaceutics · 2023Article
- Functional Role of Basolateral ClC-2 Channels in the Regulation of Duodenal Anion Secretion in Mice.Digestive diseases and sciences · 2019Article
- Lubiprostone in constipation: clinical evidence and place in therapy.Therapeutic advances in chronic disease · 2015Review
- Effects of lubiprostone on pacemaker activity of interstitial cells of cajal from the mouse colon.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014Article
- Lubiprostone decreases mouse colonic inner mucus layer thickness and alters intestinal microbiota.Digestive diseases and sciences · 2013Article
- Lubiprostone stimulates small intestinal mucin release.BMC gastroenterology · 2012Article
- Lubiprostone targets prostanoid signaling and promotes ion transporter trafficking, mucus exocytosis, and contractility.Digestive diseases and sciences · 2012Article
- May the truth be with you: lubiprostone as EP receptor agonist/ClC-2 internalizing "inhibitor".Digestive diseases and sciences · 2012Article
- Lubiprostone for the treatment of adult women with irritable bowel syndrome with constipation.Clinical medicine insights. Gastroenterology · 2012Review
- Lubiprostone for the treatment of adults with constipation and irritable bowel syndrome.Digestive diseases and sciences · 2011Review
- Lubiprostone: evaluation of the newest medication for the treatment of adult women with constipation-predominant irritable bowel syndrome.International journal of women's health · 2010Article
- Lubiprostone ameliorates the cystic fibrosis mouse intestinal phenotype.BMC gastroenterology · 2010Article
- Lubiprostone reverses the inhibitory action of morphine on intestinal secretion in guinea pig and mouse.The Journal of pharmacology and experimental therapeutics · 2010Article
- Prostaglandin E2-induced colonic secretion in patients with and without colorectal neoplasia.BMC gastroenterology · 2010Article
- ClC-2 regulation of intestinal barrier function: Translation of basic science to therapeutic target.Tissue barriersReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundLubiprostone, a bicyclic fatty acid, is used for the treatment of chronic constipation. No published study has addressed the effect of lubiprostone on intestinal ion secretion in vivo.
aimThe aim of this study was to test the hypothesis that lubiprostone augments duodenal HCO(3) (-) secretion (DBS).
methodsRat proximal duodenal loops were perfused with pH 7.0 Krebs, control vehicle (medium-chain triglycerides), or lubiprostone (0.1-10 microM). We measured DBS with flow-through pH and CO(2) electrodes, perfusate [Cl(-)] with a Cl(-) electrode, and water flux using a non-absorbable ferrocyanide marker. Some rats were pretreated with a potent, selective CFTR antagonist, CFTR(inh)-172 (1 mg/kg, ip), 1 h before experiments.
resultsPerfusion of lubiprostone concentration dependently increased DBS, whereas net Cl(-) output and net water output were only increased at 0.1 microM, compared with vehicle. CFTR(inh)-172 reduced lubiprostone (10 microM)-induced DBS increase, whereas net Cl(-) output was also unchanged. Nevertheless, CFTR(inh)-172 reduced basal net water output, which was reversed by lubiprostone. Furthermore, lubiprostone-induced DBS was inhibited by EP4 receptor antagonist, not by an EP1/2 receptor antagonist or by indomethacin pretreatment.
conclusionsIn this first study of the effect of lubiprostone on intestinal ion secretion in vivo, lubiprostone stimulated CFTR-dependent DBS without changing net Cl(-) secretion. This effect supports the hypothesis that Cl(-) secreted by CFTR is recycled across the apical membrane by anion exchangers. Recovery of water output during CFTR inhibition suggests that lubiprostone may improve the intestinal phenotype in CF patients. Furthermore, increased DBS suggests that lubiprostone may protect the duodenum from acid-induced injury via EP4 receptor activation.
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.