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 (667 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
Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety.
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: Phosphatidyl Cholines; Cholines, Phosphatidyl; Phosphatidyl Choline; Choline, Phosphatidyl; Choline Glycerophospholipids; Glycerophospholipids, Choline; Choline Phosphoglycerides; Phosphoglycerides, Choline.
Where it fits in the MeSH classification
- Broader topics
- Glycerophospholipids
- Narrower topics
- 1,2-Dipalmitoylphosphatidylcholine; Dimyristoylphosphatidylcholine; Lecithins
Related concepts
- Phosphatidic Acids
- Choline
Research landscape
PubMed indexes 41,652 records tagged with the MeSH heading “Phosphatidylcholines” (counts retrieved 2026-10-31). 3,375 of them (8.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 22,726 records.
Reviews account for 1,025 records (2.5%) and meta-analyses for 21. Randomized controlled trials number 333 (0.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 22,726 |
| 2000-2009 | 7,784 |
| 2010-2019 | 7,767 |
| 2020 onward | 3,375 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,025 | 2.5% |
| Meta-analyses | 21 | 0.1% |
| Randomized controlled trials | 333 | 0.8% |
Method: PubMed query "Phosphatidylcholines"[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 |
|---|---|---|---|---|
| High-fat diet-induced upregulation of exosomal phosphatidylcholine contributes to insulin resistance | 2021 | Research article Design not recorded in structured metadata | 230 | cc by PMID 33431899 · DOI · PMC7801461 |
| Accelerated phosphatidylcholine turnover in macrophages promotes adipose tissue inflammation in obesity | 2019 | Research article Design not recorded in structured metadata | 68 | cc by PMID 31418690 · DOI · PMC6748830 |
| Hydration Layer of Only a Few Molecules Controls Lipid Mobility in Biomimetic Membranes | 2021 | Research article Design not recorded in structured metadata | 51 | cc by PMID 34342967 · DOI · PMC8447254 |
| Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 42000749 · DOI · PMC13091796 |
High-fat diet-induced upregulation of exosomal phosphatidylcholine contributes to insulin resistance [1]
Abstract reading summary — source excerpts
- Opening excerpt
- High-fat diet (HFD) decreases insulin sensitivity.
- Closing excerpt
- Intestinal exosomes thus have potential as broad therapeutic targets.
- 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 (149 words)
High-fat diet (HFD) decreases insulin sensitivity. How high-fat diet causes insulin resistance is largely unknown. Here, we show that lean mice become insulin resistant after being administered exosomes isolated from the feces of obese mice fed a HFD or from patients with type II diabetes. HFD altered the lipid composition of exosomes from predominantly phosphatidylethanolamine (PE) in exosomes from lean animals (L-Exo) to phosphatidylcholine (PC) in exosomes from obese animals (H-Exo). Mechanistically, we show that intestinal H-Exo is taken up by macrophages and hepatocytes, leading to inhibition of the insulin signaling pathway. Moreover, exosome-derived PC binds to and activates AhR, leading to inhibition of the expression of genes essential for activation of the insulin signaling pathway, including IRS-2, and its downstream genes PI3K and Akt. Together, our results reveal HFD-induced exosomes as potential contributors to the development of insulin resistance. Intestinal exosomes thus have potential as broad therapeutic targets.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33431899 · DOI · PMC7801461
Accelerated phosphatidylcholine turnover in macrophages promotes adipose tissue inflammation in obesity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- White adipose tissue (WAT) inflammation contributes to the development of insulin resistance in obesity.
- Closing excerpt
- Our results reveal a causal link between obesity-associated increase in de novo PC synthesis, accelerated PC turnover and pro-inflammatory activation of ATMs.
- 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 (158 words)
White adipose tissue (WAT) inflammation contributes to the development of insulin resistance in obesity. While the role of adipose tissue macrophage (ATM) pro-inflammatory signalling in the development of insulin resistance has been established, it is less clear how WAT inflammation is initiated. Here, we show that ATMs isolated from obese mice and humans exhibit markers of increased rate of de novo phosphatidylcholine (PC) biosynthesis. Macrophage-specific knockout of phosphocholine cytidylyltransferase A (CCTα), the rate-limiting enzyme of de novo PC biosynthesis pathway, alleviated obesity-induced WAT inflammation and insulin resistance. Mechanistically, CCTα-deficient macrophages showed reduced ER stress and inflammation in response to palmitate. Surprisingly, this was not due to lower exogenous palmitate incorporation into cellular PCs. Instead, CCTα-null macrophages had lower membrane PC turnover, leading to elevated membrane polyunsaturated fatty acid levels that negated the pro-inflammatory effects of palmitate. Our results reveal a causal link between obesity-associated increase in de novo PC synthesis, accelerated PC turnover and pro-inflammatory activation of ATMs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31418690 · DOI · PMC6748830
Hydration Layer of Only a Few Molecules Controls Lipid Mobility in Biomimetic Membranes [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Self-assembly of biomembranes results from the intricate interactions between water and the lipids' hydrophilic head groups.
- Closing excerpt
- Finally, the strong dependence of lipid mobility on the number of hydrating water molecules opens up an application potential for SLBs as very precise, nanoscale hydration sensors.
- 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 (214 words)
Self-assembly of biomembranes results from the intricate interactions between water and the lipids' hydrophilic head groups. Therefore, the lipid-water interplay strongly contributes to modulating membrane architecture, lipid diffusion, and chemical activity. Here, we introduce a new method of obtaining dehydrated, phase-separated, supported lipid bilayers (SLBs) solely by controlling the decrease of their environment's relative humidity. This facilitates the study of the structure and dynamics of SLBs over a wide range of hydration states. We show that the lipid domain structure of phase-separated SLBs is largely insensitive to the presence of the hydration layer. In stark contrast, lipid mobility is drastically affected by dehydration, showing a 6-fold decrease in lateral diffusion. At the same time, the diffusion activation energy increases approximately 2-fold for the dehydrated membrane. The obtained results, correlated with the hydration structure of a lipid molecule, revealed that about six to seven water molecules directly hydrating the phosphocholine moiety play a pivotal role in modulating lipid diffusion. These findings could provide deeper insights into the fundamental reactions where local dehydration occurs, for instance during cell-cell fusion, and help us better understand the survivability of anhydrobiotic organisms. Finally, the strong dependence of lipid mobility on the number of hydrating water molecules opens up an application potential for SLBs as very precise, nanoscale hydration sensors.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34342967 · DOI · PMC8447254
Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Mitochondrial dysfunction is a prominent hallmark of aging contributing to the decline of metabolic plasticity in late life.
- Closing excerpt
- We thus describe a previously unrecognized natural driver of mitochondrial decline in aging that is malleable by dietary interventions.
- 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 (146 words)
Mitochondrial dysfunction is a prominent hallmark of aging contributing to the decline of metabolic plasticity in late life. While genetic distortions of mitochondrial integrity elicit premature aging, the mechanisms leading to "natural" aging of mitochondria are less clear. Here we use proteomics, lipidomics, genetics and functional tests in wild type Caenorhabditis elegans and long-lived clk-1(qm30) and isp-1(qm150) mitochondrial mutants to identify molecular pathways that support longevity amid persistent mitochondrial inefficiency. These tests and subsequent transcriptomics and metabolomics analyses in humans reveal aging-associated decline of phosphatidylcholine synthesis as a trigger of mitochondrial network disruption, which contributes to mitochondrial dysfunction during normal aging. Moreover, ectopic boosting of phosphatidylcholine levels via diet restores late life mitochondrial integrity in vivo in nematodes and reinstates metabolic resilience in human cell culture tests. We thus describe a previously unrecognized natural driver of mitochondrial decline in aging that is malleable by dietary interventions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42000749 · DOI · PMC13091796
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 The plasma lecithins:cholesterol acyltransferase reaction [5]
- Research article The critical role of phosphatidylcholine and phosphatidylethanolamine metabolism in health and disease [6]
- Research article Signaling through phosphatidylcholine breakdown [7]
- Research article Phases and phase transitions of the phosphatidylcholines [8]
- Research article The Kennedy pathway--De novo synthesis of phosphatidylethanolamine and phosphatidylcholine [9]
- Research article The mechanisms of lysophosphatidylcholine in the development of diseases [10]
References
- Kumar A, Sundaram K, Mu J, Dryden GW, Sriwastva MK, Lei C, et al.. High-fat diet-induced upregulation of exosomal phosphatidylcholine contributes to insulin resistance. . 2021. PMID 33431899 · DOI · PMC7801461
- Petkevicius K, Virtue S, Bidault G, Jenkins B, Çubuk C, Morgantini C, et al.. Accelerated phosphatidylcholine turnover in macrophages promotes adipose tissue inflammation in obesity. . 2019. PMID 31418690 · DOI · PMC6748830
- Chattopadhyay M, Krok E, Orlikowska H, Schwille P, Franquelim HG, Piatkowski L. Hydration Layer of Only a Few Molecules Controls Lipid Mobility in Biomimetic Membranes. . 2021. PMID 34342967 · DOI · PMC8447254
- Poliezhaieva T, Li Y, Chaudhari PS, Isildak U, Alonso-Pernas P, Valentim IS, et al.. Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging. . 2026. PMID 42000749 · DOI · PMC13091796
- Glomset JA. The plasma lecithins:cholesterol acyltransferase reaction. J Lipid Res. 1968. PMID 4868699 · DOI
- van der Veen JN, Kennelly JP, Wan S, Vance JE, Vance DE, Jacobs RL. The critical role of phosphatidylcholine and phosphatidylethanolamine metabolism in health and disease. Biochim Biophys Acta Biomembr. 2017. PMID 28411170 · DOI
- Exton JH. Signaling through phosphatidylcholine breakdown. J Biol Chem. 1990. PMID 2104616 · DOI
- Koynova R, Caffrey M. Phases and phase transitions of the phosphatidylcholines. Biochim Biophys Acta. 1998. PMID 9666088 · DOI
- Gibellini F, Smith TK. The Kennedy pathway--De novo synthesis of phosphatidylethanolamine and phosphatidylcholine. IUBMB Life. 2010. PMID 20503434 · DOI
- Liu P, Zhu W, Chen C, Yan B, Zhu L, Chen X, et al.. The mechanisms of lysophosphatidylcholine in the development of diseases. Life Sci. 2020. PMID 32084434 · DOI
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.