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 (735 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 common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.
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: Acid, Palmitic; Hexadecanoic Acid; Acid, Hexadecanoic; Calcium Palmitate; Palmitate, Calcium; Sodium Palmitate; Palmitate, Sodium.
Where it fits in the MeSH classification
- Broader topics
- Palmitic Acids
Research landscape
PubMed indexes 7,456 records tagged with the MeSH heading “Palmitic Acid” (counts retrieved 2026-10-31). 1,337 of them (17.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,559 records.
Reviews account for 184 records (2.5%) and meta-analyses for 5. Randomized controlled trials number 110 (1.5%) 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 | 2,559 |
| 2000-2009 | 1,535 |
| 2010-2019 | 2,025 |
| 2020 onward | 1,337 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 184 | 2.5% |
| Meta-analyses | 5 | 0.1% |
| Randomized controlled trials | 110 | 1.5% |
Method: PubMed query "Palmitic Acid"[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 |
|---|---|---|---|---|
| The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms | 2019 | Review article Design not recorded in structured metadata | 411 | cc by PMID 31363792 · DOI · PMC6813288 |
| Saturated palmitic acid induces myocardial inflammatory injuries through direct binding to TLR4 accessory protein MD2 | 2017 | Research article Design not recorded in structured metadata | 206 | cc by PMID 28045026 · DOI · PMC5216130 |
| Exosomes derived from palmitic acid-treated hepatocytes induce fibrotic activation of hepatic stellate cells | 2017 | Research article Design not recorded in structured metadata | 194 | cc by PMID 28623272 · DOI · PMC5473841 |
| CD36 enhances sensitivity of triple negative breast cancer cells to palmitate-induced ferroptosis | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41672971 · DOI · PMC12920903 |
The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Palmitic acid is a saturated fatty acid whose blood concentration is elevated in obese patients.
- Closing excerpt
- Due to the high importance of macrophages and the production of proinflammatory cytokines by them, this work mainly focuses on these cells.
- 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 (200 words)
Palmitic acid is a saturated fatty acid whose blood concentration is elevated in obese patients. This causes inflammatory responses, where toll-like receptors (TLR), TLR2 and TLR4, play an important role. Nevertheless, palmitic acid is not only a TLR agonist. In the cell, this fatty acid is converted into phospholipids, diacylglycerol and ceramides. They trigger the activation of various signaling pathways that are common for LPS-mediated TLR4 activation. In particular, metabolic products of palmitic acid affect the activation of various PKCs, ER stress and cause an increase in ROS generation. Thanks to this, palmitic acid also strengthens the TLR4-induced signaling. In this review, we discuss the mechanisms of inflammatory response induced by palmitic acid. In particular, we focus on describing its effect on ER stress and IRE1α, and the mechanisms of NF-κB activation. We also present the mechanisms of inflammasome NLRP3 activation and the effect of palmitic acid on enhanced inflammatory response by increasing the expression of FABP4/aP2. Finally, we focus on the consequences of inflammatory responses, in particular, the effect of TNF-α, IL-1β and IL-6 on insulin resistance. Due to the high importance of macrophages and the production of proinflammatory cytokines by them, this work mainly focuses on these cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31363792 · DOI · PMC6813288
Saturated palmitic acid induces myocardial inflammatory injuries through direct binding to TLR4 accessory protein MD2 [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Obesity increases the risk for a number of diseases including cardiovascular diseases and type 2 diabetes.
- Closing excerpt
- We conclude that PA is a crucial contributor to obesity-associated myocardial injury, which is likely regulated via its direct binding to MD2.
- 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 (147 words)
Obesity increases the risk for a number of diseases including cardiovascular diseases and type 2 diabetes. Excess saturated fatty acids (SFAs) in obesity play a significant role in cardiovascular diseases by activating innate immunity responses. However, the mechanisms by which SFAs activate the innate immune system are not fully known. Here we report that palmitic acid (PA), the most abundant circulating SFA, induces myocardial inflammatory injury through the Toll-like receptor 4 (TLR4) accessory protein MD2 in mouse and cell culture experimental models. Md2 knockout mice are protected against PA- and high-fat diet-induced myocardial injury. Studies of cell surface binding, cell-free protein-protein interactions and molecular docking simulations indicate that PA directly binds to MD2, supporting a mechanism by which PA activates TLR4 and downstream inflammatory responses. We conclude that PA is a crucial contributor to obesity-associated myocardial injury, which is likely regulated via its direct binding to MD2.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28045026 · DOI · PMC5216130
Exosomes derived from palmitic acid-treated hepatocytes induce fibrotic activation of hepatic stellate cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Non-alcoholic fatty liver disease (NAFLD) is a dominant cause of chronic liver disease, but the exact mechanism of progression from simple steatosis to nonalcoholic steatohepatitis (NASH) remains unknown.
- Closing excerpt
- Therefore, exosomes may have important roles in the crosstalk between hepatocytes and HSCs in the progression from simple steatosis to NASH.
- 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 (194 words)
Non-alcoholic fatty liver disease (NAFLD) is a dominant cause of chronic liver disease, but the exact mechanism of progression from simple steatosis to nonalcoholic steatohepatitis (NASH) remains unknown. Here, we investigated the role of exosomes in NAFLD progression. Exosomes were isolated from a human hepatoma cell line treated with palmitic acid (PA) and their miRNA profiles examined by microarray. The human hepatic stellate cell (HSC) line (LX-2) was then treated with exosome isolated from hepatocytes. Compared with controls, PA-treated hepatocytes displayed significantly increased CD36 and exosome production. The microarray analysis showed there to be distinctive miRNA expression patterns between exosomes from vehicle- and PA-treated hepatocytes. When LX-2 cells were cultured with exosomes from PA-treated hepatocytes, the expression of genes related to the development of fibrosis were significantly amplified compared to those treated with exosomes from vehicle-treated hepatocytes. In conclusion, PA treatment enhanced the production of exosomes in these hepatocytes and changed their exosomal miRNA profile. Moreover, exosomes derived from PA-treated hepatocytes caused an increase in the expression levels of fibrotic genes in HSCs. Therefore, exosomes may have important roles in the crosstalk between hepatocytes and HSCs in the progression from simple steatosis to NASH.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28623272 · DOI · PMC5473841
CD36 enhances sensitivity of triple negative breast cancer cells to palmitate-induced ferroptosis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Ferroptosis is a newly identified programmed cell death induced by iron-driven lipid peroxidation and implicated as a potential approach for tumor treatment.
- Closing excerpt
- Altogether, these data provide evidence for an essential role of the CD36 protein in the ferroptotic process induced by the saturated fatty acid PA, opening potential new therapeutic approaches promoting ferroptosis in the most aggressive breast cancers.
- 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 (194 words)
Ferroptosis is a newly identified programmed cell death induced by iron-driven lipid peroxidation and implicated as a potential approach for tumor treatment. Breast tumors develop in a complex microenvironment whose main component is adipose tissue and gain aggressiveness through increased fatty acid uptake. Here, we demonstrated that palmitic acid (PA) induced ferroptosis in triple negative breast cancers (TNBC). We found that PA increases the protein expression levels of the long-chain fatty acid transporter CD36, leading to increased lipid uptake. Mechanistically, overexpression of CD36 increases lipid peroxidation, mitochondrial ROS production, the labile iron pool, and especially Fe2+ content. Additionally, we found increased expression of ferroptotic target genes (HMOX1, ACSL1, SAT1) and decreased of anti-ferroptotic genes (GPX4 and FSP1) in TNBC following PA exposure. Overexpression of CD36 did not induce ferroptosis in estrogen receptor positive breast cancer. Clinically, higher CD36 expression correlated with the luminal androgen receptor (LAR) subtype of TNBC, known to exhibit a higher sensitivity to ferroptosis. Altogether, these data provide evidence for an essential role of the CD36 protein in the ferroptotic process induced by the saturated fatty acid PA, opening potential new therapeutic approaches promoting ferroptosis in the most aggressive breast cancers.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41672971 · DOI · PMC12920903
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 Palmitoylation: policing protein stability and traffic [5]
- Research article Palmitic and Oleic Acid: The Yin and Yang of Fatty Acids in Type 2 Diabetes Mellitus [6]
- Research article Protein palmitoylation by a family of DHHC protein S-acyltransferases [7]
- Research article The physiology of protein S-acylation [8]
- Research article Protein palmitoylation and subcellular trafficking [9]
- Research article DHHC palmitoyl transferases: substrate interactions and (patho)physiology [10]
References
- Korbecki J, Bajdak-Rusinek K. The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms. . 2019. PMID 31363792 · DOI · PMC6813288
- Wang Y, Qian Y, Fang Q, Zhong P, Li W, Wang L, et al.. Saturated palmitic acid induces myocardial inflammatory injuries through direct binding to TLR4 accessory protein MD2. . 2017. PMID 28045026 · DOI · PMC5216130
- Lee YS, Kim SY, Ko E, Lee JH, Yi HS, Yoo YJ, et al.. Exosomes derived from palmitic acid-treated hepatocytes induce fibrotic activation of hepatic stellate cells. . 2017. PMID 28623272 · DOI · PMC5473841
- Closset L, Foy JP, Louadj L, Pramil E, Marangoni E, Bieche I, et al.. CD36 enhances sensitivity of triple negative breast cancer cells to palmitate-induced ferroptosis. . 2026. PMID 41672971 · DOI · PMC12920903
- Linder ME, Deschenes RJ. Palmitoylation: policing protein stability and traffic. Nat Rev Mol Cell Biol. 2007. PMID 17183362 · DOI
- Palomer X, Pizarro-Delgado J, Barroso E, Vázquez-Carrera M. Palmitic and Oleic Acid: The Yin and Yang of Fatty Acids in Type 2 Diabetes Mellitus. Trends Endocrinol Metab. 2018. PMID 29290500 · DOI
- Mitchell DA, Vasudevan A, Linder ME, Deschenes RJ. Protein palmitoylation by a family of DHHC protein S-acyltransferases. J Lipid Res. 2006. PMID 16582420 · DOI
- Chamberlain LH, Shipston MJ. The physiology of protein S-acylation. Physiol Rev. 2015. PMID 25834228 · DOI · PMC4551212
- Aicart-Ramos C, Valero RA, Rodriguez-Crespo I. Protein palmitoylation and subcellular trafficking. Biochim Biophys Acta. 2011. PMID 21819967 · DOI
- Greaves J, Chamberlain LH. DHHC palmitoyl transferases: substrate interactions and (patho)physiology. Trends Biochem Sci. 2011. PMID 21388813 · 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.