Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (749 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: 2-Hydroxy-N,N,N-trimethylethanaminium; Choline Bitartrate; Bitartrate, Choline; Choline Chloride; Chloride, Choline; Choline Citrate; Citrate, Choline; Choline O-Sulfate.
Where it fits in the MeSH classification
- Broader topics
- Ethanolamines; Trimethyl Ammonium Compounds; Quaternary Ammonium Compounds
- Narrower topics
- Platelet Activating Factor; Benzoylcholine; Carbachol; Cytidine Diphosphate Choline; Phosphorylcholine; Propylbenzilylcholine Mustard; Succinylcholine; Thiocholine
Research landscape
PubMed indexes 56,670 records tagged with the MeSH heading “Choline” (counts retrieved 2026-10-31). 4,211 of them (7.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 35,896 records.
Reviews account for 2,909 records (5.1%) and meta-analyses for 133. Randomized controlled trials number 1,184 (2.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 35,896 |
| 2000-2009 | 8,960 |
| 2010-2019 | 7,603 |
| 2020 onward | 4,211 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,909 | 5.1% |
| Meta-analyses | 133 | 0.2% |
| Randomized controlled trials | 1,184 | 2.1% |
Method: PubMed query "Choline"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Biased signaling due to oligomerization of the G protein-coupled platelet-activating factor receptor | 2022 | Research article Design not recorded in structured metadata | 68 | cc by PMID 36289206 · DOI · PMC9606269 |
| Gut microbe-targeted choline trimethylamine lyase inhibition improves obesity via rewiring of host circadian rhythms | 2022 | Research article Design not recorded in structured metadata | 57 | cc by PMID 35072627 · DOI · PMC8813054 |
| Dynamics of Choline-Containing Phospholipids in Traumatic Brain Injury and Associated Comorbidities | 2021 | Review article Design not recorded in structured metadata | 53 | cc by PMID 34768742 · DOI · PMC8583393 |
| Diazoxide Choline Extended-release Tablets in Prader-Willi Syndrome: A Randomized, Double-blind, Withdrawal Period Study | 2026 | Randomized controlled trial Design not recorded in structured metadata | 7 | cc by PMID 41482637 · DOI · PMC13183442 |
Biased signaling due to oligomerization of the G protein-coupled platelet-activating factor receptor [1]
Abstract reading summary — source excerpts
- Opening excerpt
- G protein-coupled receptors (GPCRs) are important drug targets that mediate various signaling pathways by activating G proteins and engaging β-arrestin proteins.
- Closing excerpt
- Our results highlight a mechanism involved in the control of receptor signaling, and thereby provide important insights into the relationship between GPCR oligomerization and downstream signaling.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (136 words)
G protein-coupled receptors (GPCRs) are important drug targets that mediate various signaling pathways by activating G proteins and engaging β-arrestin proteins. Despite its importance for the development of therapeutics with fewer side effects, the underlying mechanism that controls the balance between these signaling modes of GPCRs remains largely unclear. Here, we show that assembly into dimers and oligomers can largely influence the signaling mode of the platelet-activating factor receptor (PAFR). Single-particle analysis results show that PAFR can form oligomers at low densities through two possible dimer interfaces. Stabilization of PAFR oligomers through cross-linking increases G protein activity, and decreases β-arrestin recruitment and agonist-induced internalization significantly. Reciprocally, β-arrestin prevents PAFR oligomerization. Our results highlight a mechanism involved in the control of receptor signaling, and thereby provide important insights into the relationship between GPCR oligomerization and downstream signaling.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36289206 · DOI · PMC9606269
Gut microbe-targeted choline trimethylamine lyase inhibition improves obesity via rewiring of host circadian rhythms [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Obesity has repeatedly been linked to reorganization of the gut microbiome, yet to this point obesity therapeutics have been targeted exclusively toward the human host.
- Closing excerpt
- This work also demonstrates that gut microbe-targeted enzyme inhibitors have potential as anti-obesity therapeutics.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Obesity has repeatedly been linked to reorganization of the gut microbiome, yet to this point obesity therapeutics have been targeted exclusively toward the human host. Here, we show that gut microbe-targeted inhibition of the trimethylamine N-oxide (TMAO) pathway protects mice against the metabolic disturbances associated with diet-induced obesity (DIO) or leptin deficiency (Lepob/ob). Small molecule inhibition of the gut microbial enzyme choline TMA-lyase (CutC) does not reduce food intake but is instead associated with alterations in the gut microbiome, improvement in glucose tolerance, and enhanced energy expenditure. We also show that gut microbial CutC inhibition is associated with reorganization of host circadian control of both phosphatidylcholine and energy metabolism. This study underscores the relationship between microbe and host metabolism and provides evidence that gut microbe-derived trimethylamine (TMA) is a key regulator of the host circadian clock. This work also demonstrates that gut microbe-targeted enzyme inhibitors have potential as anti-obesity therapeutics.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35072627 · DOI · PMC8813054
Dynamics of Choline-Containing Phospholipids in Traumatic Brain Injury and Associated Comorbidities [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The incidences of traumatic brain injuries (TBIs) are increasing globally because of expanding population and increased dependencies on motorized vehicles and machines.
- Closing excerpt
- Overall, this review determines the theranostic potential of choline phospholipids and provides new insights in the management of TBI.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (216 words)
The incidences of traumatic brain injuries (TBIs) are increasing globally because of expanding population and increased dependencies on motorized vehicles and machines. This has resulted in increased socio-economic burden on the healthcare system, as TBIs are often associated with mental and physical morbidities with lifelong dependencies, and have severely limited therapeutic options. There is an emerging need to identify the molecular mechanisms orchestrating these injuries to life-long neurodegenerative disease and a therapeutic strategy to counter them. This review highlights the dynamics and role of choline-containing phospholipids during TBIs and how they can be used to evaluate the severity of injuries and later targeted to mitigate neuro-degradation, based on clinical and preclinical studies. Choline-based phospholipids are involved in maintaining the structural integrity of the neuronal/glial cell membranes and are simultaneously the essential component of various biochemical pathways, such as cholinergic neuronal transmission in the brain. Choline or its metabolite levels increase during acute and chronic phases of TBI because of excitotoxicity, ischemia and oxidative stress; this can serve as useful biomarker to predict the severity and prognosis of TBIs. Moreover, the effect of choline-replenishing agents as a post-TBI management strategy has been reviewed in clinical and preclinical studies. Overall, this review determines the theranostic potential of choline phospholipids and provides new insights in the management of TBI.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34768742 · DOI · PMC8583393
Diazoxide Choline Extended-release Tablets in Prader-Willi Syndrome: A Randomized, Double-blind, Withdrawal Period Study [4]
Abstract reading summary — source excerpts
- Opening excerpt
- ContextThe hallmark condition of Prader-Willi syndrome, a rare, genetic neurobehavioral/metabolic disorder, is life-threatening hyperphagia.
- Closing excerpt
- DCCR appears to offer meaningful therapeutic benefits for people with Prader-Willi syndrome.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (247 words)
ContextThe hallmark condition of Prader-Willi syndrome, a rare, genetic neurobehavioral/metabolic disorder, is life-threatening hyperphagia.ObjectiveWe assessed the efficacy and safety of diazoxide choline extended-release (DCCR) tablets for the treatment of hyperphagia in adults and children four years of age and older with Prader-Willi syndrome.MethodsWe conducted a 16-week, randomized withdrawal study in children and adults with Prader-Willi syndrome and hyperphagia. Participants who previously completed randomized (13-week DCCR or placebo) and open-label (2.5-4.5 years DCCR) studies were randomized 1:1 to receive once-daily DCCR or placebo. The primary endpoint was Hyperphagia Questionnaire for Clinical Trials (HQ-CT) total score change from baseline to 16 weeks. Secondary endpoints included Clinical Global Impression of Severity (CGI-S) and Improvement (CGI-I); exploratory endpoints included weight and body mass index (BMI) z-score.ResultsSeventy-seven participants were randomized (DCCR:38; placebo:39). Statistically significant increases in HQ-CT from baseline to week 16 were observed with placebo vs DCCR [least square (LS) mean (standard error) change 7.6 (1.09)] with placebo and 2.6 (1.12) with DCCR; P = .0022. CGI scores favored DCCR but were not significantly changed. Consistent with the hyperphagia response, the placebo cohort gained more weight and increased their BMI z-score more than the DCCR cohort [LS mean weight difference (95% confidence interval) -1.6 kg (-3.1, -0.1)]; LS mean z-score difference was -0.09 (-0.17, -0.01). Adverse events were similar with both treatments, with no serious adverse events in the DCCR arm.ConclusionContinued DCCR treatment was superior to placebo for hyperphagia. DCCR appears to offer meaningful therapeutic benefits for people with Prader-Willi syndrome.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41482637 · DOI · PMC13183442
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Choline: an essential nutrient for public health [5]
- Research article Cholinesterase inhibitors as Alzheimer's therapeutics (Review) [6]
- Research article Choline and betaine in health and disease [7]
- Research article The role of phosphatidylcholine and choline metabolites to cell proliferation and survival [8]
- Research article The role of 11C-choline and 18F-fluorocholine positron emission tomography (PET) and PET/CT in prostate cancer: a systematic review and meta-analysis [9]
- Research article Dietary Choline Intake: Current State of Knowledge Across the Life Cycle [10]
References
- Liu J, Tang H, Xu C, Zhou S, Zhu X, Li Y, et al.. Biased signaling due to oligomerization of the G protein-coupled platelet-activating factor receptor. . 2022. PMID 36289206 · DOI · PMC9606269
- Schugar RC, Gliniak CM, Osborn LJ, Massey W, Sangwan N, Horak A, et al.. Gut microbe-targeted choline trimethylamine lyase inhibition improves obesity via rewiring of host circadian rhythms. . 2022. PMID 35072627 · DOI · PMC8813054
- Javaid S, Farooq T, Rehman Z, Afzal A, Ashraf W, Rasool MF, et al.. Dynamics of Choline-Containing Phospholipids in Traumatic Brain Injury and Associated Comorbidities. . 2021. PMID 34768742 · DOI · PMC8583393
- Miller JL, Bridges N, Felner EI, Salehi P, Yanovski JA, Stevenson DA, et al.. Diazoxide Choline Extended-release Tablets in Prader-Willi Syndrome: A Randomized, Double-blind, Withdrawal Period Study. . 2026. PMID 41482637 · DOI · PMC13183442
- Zeisel SH, da Costa KA. Choline: an essential nutrient for public health. Nutr Rev. 2009. PMID 19906248 · DOI · PMC2782876
- Sharma K. Cholinesterase inhibitors as Alzheimer's therapeutics (Review). Mol Med Rep. 2019. PMID 31257471 · DOI · PMC6625431
- Ueland PM. Choline and betaine in health and disease. J Inherit Metab Dis. 2011. PMID 20446114 · DOI
- Ridgway ND. The role of phosphatidylcholine and choline metabolites to cell proliferation and survival. Crit Rev Biochem Mol Biol. 2013. PMID 23350810 · DOI
- Umbehr MH, Müntener M, Hany T, Sulser T, Bachmann LM. The role of 11C-choline and 18F-fluorocholine positron emission tomography (PET) and PET/CT in prostate cancer: a systematic review and meta-analysis. Eur Urol. 2013. PMID 23628493 · DOI
- Wiedeman AM, Barr SI, Green TJ, Xu Z, Innis SM, Kitts DD. Dietary Choline Intake: Current State of Knowledge Across the Life Cycle. Nutrients. 2018. PMID 30332744 · DOI · PMC6213596
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.