ArticleBritish journal of pharmacology2012
Inhibiting fatty acid amide hydrolase normalizes endotoxin-induced enhanced gastrointestinal motility in mice.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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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.
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Who cites it
26 citing papers in PubMed, 59 citations in OpenAlex.
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- Randomized pharmacodynamic and pharmacogenetic trial of dronabinol effects on colon transit in irritable bowel syndrome-diarrhea.Neurogastroenterology and motility · 2012Trial
- Prospects in the Use ofBiotech (Basel (Switzerland)) · 2024Review
- FAAH inhibitor URB597 shows anti-hyperalgesic action and increases brain and intestinal tissues fatty acid amides in a model of CRFNeurogastroenterology and motility · 2024Article
- Supporting gut health with medicinal cannabis in people with advanced cancer: potential benefits and challenges.British journal of cancer · 2024Review
- Cannabidiol and Intestinal Motility: a Systematic Review.Current developments in nutrition · 2023Review
- Inhibiting Fatty Acid Amide Hydrolase Ameliorates Enteropathy in Diabetic Mice: A Cannabinoid 1 Receptor Mediated Mechanism.Veterinary sciences · 2022Article
- Multi-omics analysis reveals the metabolic regulators of duodenal low-grade inflammation in a functional dyspepsia model.Frontiers in immunology · 2022Article
- Cannabis and Cannabis Derivatives for Abdominal Pain Management in Inflammatory Bowel Disease.Medical cannabis and cannabinoids · 2021Review
- Recommendations for evaluation of bladder and bowel function in pre-clinical spinal cord injury research.The journal of spinal cord medicine · 2020Review
- Cannabinoid Antagonist Drug Discrimination in Nonhuman Primates.The Journal of pharmacology and experimental therapeutics · 2020Article
- Non-endocannabinoid N-acylethanolamines and 2-monoacylglycerols in the intestine.British journal of pharmacology · 2019Review
- Multiple endocannabinoid-mediated mechanisms in the regulation of energy homeostasis in brain and peripheral tissues.Cellular and molecular life sciences : CMLS · 2019Review
- Chinese Herbal Medicine (MaZiRenWan) Improves Bowel Movement in Functional Constipation Through Down-Regulating Oleamide.Frontiers in pharmacology · 2019Article
- Toll-Like Receptor 4 Modulates Small Intestine Neuromuscular Function through Nitrergic and Purinergic Pathways.Frontiers in pharmacology · 2017Article
- The gastrointestinal tract - a central organ of cannabinoid signaling in health and disease.Neurogastroenterology and motility · 2016Review
- The Role of the Endocannabinoid System in the Brain-Gut Axis.Gastroenterology · 2016Review
- Monoglyceride lipase deficiency causes desensitization of intestinal cannabinoid receptor type 1 and increased colonic μ-opioid receptor sensitivity.British journal of pharmacology · 2015Article
- Inhibiting endocannabinoid biosynthesis: a novel approach to the treatment of constipation.British journal of pharmacology · 2015Article
- Sulfonyl fluorides as privileged warheads in chemical biology.Chemical science · 2015Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
background and purposeGastrointestinal (GI) motility is regulated in part by fatty acid ethanolamides (FAEs), including the endocannabinoid (EC) anandamide (AEA). The actions of FAEs are terminated by fatty acid amide hydrolase (FAAH). We investigated the actions of the novel FAAH inhibitor AM3506 on normal and enhanced GI motility. EXPERIMENTAL APPROACH: We examined the effect of AM3506 on electrically-evoked contractility in vitro and GI transit and colonic faecal output in vivo, in normal and FAAH-deficient mice treated with saline or LPS (100 µg·kg(-1), i.p.), in the presence and absence of cannabinoid (CB) receptor antagonists. mRNA expression was measured by quantitative real time-PCR, EC levels by liquid chromatography-MS and FAAH activity by the conversion of [(3)H]-AEA to [(3)H]-ethanolamine in intestinal extracts. FAAH expression was examined by immunohistochemistry. KEY
resultsFAAH was dominantly expressed in the enteric nervous system; its mRNA levels were higher in the ileum than the colon. LPS enhanced ileal contractility in the absence of overt inflammation. AM3506 reversed the enhanced electrically-evoked contractions of the ileum through CB(1) and CB(2) receptors. LPS increased the rate of upper GI transit and faecal output. AM3506 normalized the enhanced GI transit through CB(1) and CB(2) receptors and faecal output through CB(1) receptors. LPS did not increase GI transit in FAAH-deficient mice. CONCLUSIONS AND IMPLICATIONS: Inhibiting FAAH normalizes various parameters of GI dysmotility in intestinal pathophysiology. Inhibition of FAAH represents a new approach to the treatment of disordered intestinal motility.
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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.