GO:0045485 omega-6 fatty acid desaturase activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0045485 (omega-6 fatty acid desaturase activity) is a molecular_function term defined as the catalysis of the introduction of an omega-6 double bond into the fatty acid hydrocarbon chain.
• The enzymes carrying this activity, notably delta-6 desaturase (FADS2) and delta-5 desaturase (FADS1), convert dietary linoleic acid toward arachidonic acid and other omega-6 polyunsaturated fatty acids.
• Desaturase activity is not fixed: it declines with age in rat liver microsomes and is altered in hereditary hypertriglyceridemic rats.
• Omega-6 desaturase activity is linked to human metabolic outcomes, including incident metabolic syndrome in relation to serum zinc and a proposed desaturase hypothesis for atherosclerosis.
• FADS1-dependent omega-6 fatty acid metabolic disruption has been implicated in anesthesia/surgery-induced cognitive impairment in aged mice.
• In human sebocytes, linoleic acid and arachidonic acid regulate delta-6 desaturase-2 expression and enhance proinflammatory activity without affecting lipogenesis.
Description
GO:0045485, omega-6 fatty acid desaturase activity, is a Gene Ontology molecular_function term describing the catalysis of the introduction of an omega-6 double bond into the fatty acid hydrocarbon chain. This activity sits at the center of polyunsaturated fatty acid (PUFA) metabolism, where it helps convert dietary essential fatty acids into longer, more unsaturated products. The desaturase hypothesis for atherosclerosis frames these enzymes as Janus-faced actors in omega-6 and omega-3 PUFA metabolism, meaning their balance can influence both protective and harmful lipid pathways. For researchers, GO:0045485 is therefore not an abstract annotation but a functional node that connects diet, membrane lipid composition, eicosanoid signaling, and disease risk. The activity is commonly studied through delta-6 desaturase and delta-5 desaturase steps, which are encoded by FADS2 and FADS1 respectively in humans. Human nutrition perspectives emphasize that omega-3 and omega-6 fatty acid biochemistry depends on these desaturation and elongation steps, making the enzymes that carry GO:0045485 central to interpreting fatty acid profiles. Experimental work in animal models shows that this activity is dynamic: delta-6 desaturase activity and fatty acid composition of rat liver microsomes change with aging, and delta-6 desaturase activity and gene expression differ in hereditary hypertriglyceridemic rats alongside glucose turnover. Because omega-6 fatty acid desaturase activity influences the balance of arachidonic acid and other omega-6 PUFAs, it has been examined in metabolic syndrome, macrophage cardiolipin remodeling, sebocyte inflammation, and aged-mouse cognitive impairment after anesthesia/surgery. These studies make GO:0045485 a practical target for CRISPR-based cell models that test causality rather than correlation.
omega-6 fatty acid desaturase activity At A Glance
| GO ID | GO:0045485 |
|---|---|
| GO term | omega-6 fatty acid desaturase activity |
| Ontology | molecular_function |
| Synonym | none listed |
| Definition | Catalysis of the introduction of an omega-6 double bond into the fatty acid hydrocarbon chain. |
| Major function | Desaturation of fatty acid hydrocarbon chains at an omega-6 position, contributing to omega-6 PUFA synthesis. |
| Representative enzymes | Delta-6 desaturase (FADS2) and delta-5 desaturase (FADS1) steps in PUFA metabolism [1,2]. |
| Physiological context | Influences membrane fatty acid composition and eicosanoid precursor availability [1,2]. |
| Disease relevance | Linked to atherosclerosis, metabolic syndrome, inflammation, and cognitive impairment in models [1,4,6,8]. |
What Is GO:0045485?
In plain terms, GO:0045485 describes the catalytic activity that inserts an omega-6 double bond into a fatty acid hydrocarbon chain. The QuickGO definition states: Catalysis of the introduction of an omega-6 double bond into the fatty acid hydrocarbon chain. This is a molecular_function annotation, meaning it describes what a gene product does at the biochemical level rather than where it acts or which pathway it belongs to. The term has no listed synonyms in the provided QuickGO data. Enzymes annotated with this activity act on fatty acyl substrates and contribute to the production of omega-6 polyunsaturated fatty acids such as arachidonic acid.
Why Is omega-6 fatty acid desaturase activity Important in Cell Biology?
GO:0045485 matters because the introduction of omega-6 double bonds determines the abundance of downstream omega-6 PUFAs, including arachidonic acid, which is a precursor for inflammatory and vascular signaling lipids. The desaturase hypothesis for atherosclerosis explicitly proposes that these enzymes are Janus-faced in omega-6 and omega-3 PUFA metabolism, so their activity can shift the balance between competing lipid mediators. Human nutrition studies reinforce that omega-3 and omega-6 fatty acid biochemistry cannot be interpreted without the desaturation steps. Because the activity changes with age, genetic background, and metabolic state, it is a plausible mechanistic link between diet, lipid profiles, and disease. It is also experimentally tractable: delta-6 desaturase activity and gene expression can be measured in tissue models, and FADS1-dependent omega-6 metabolic disruption can be modeled in aged mice.
• Defines a key enzymatic step in omega-6 PUFA biosynthesis and arachidonic acid production.
• Shapes membrane fatty acid composition and the pool of eicosanoid precursors [1,2].
• Declines with age in rat liver microsomes, linking aging to altered lipid metabolism.
• Is altered in hereditary hypertriglyceridemic rats together with glucose turnover.
• Associates with incident metabolic syndrome in human studies of desaturase activities and serum zinc.
• Contributes to cardiolipin remodeling differences between omega-3 and omega-6 fatty acids in activated macrophages.
• Regulates proinflammatory activity in human sebocytes without affecting lipogenesis.
• FADS1-dependent omega-6 metabolic disruption is implicated in anesthesia/surgery-induced cognitive impairment in aged mice.
• Provides a mechanistic hypothesis for atherosclerosis through the desaturase hypothesis.
• Offers a tractable target for CRISPR knockout, point-mutation, knock-in, and overexpression cell models.
Molecular Mechanism of omega-6 fatty acid desaturase activity
Substrate recognition and fatty acid chain binding
In simple terms: The enzyme must first grab the correct fatty acid chain before it can add a double bond.
Omega-6 fatty acid desaturase activity acts on fatty acid hydrocarbon chains, and the QuickGO definition specifies the introduction of an omega-6 double bond into that chain. In PUFA metabolism, this activity is represented by delta-6 and delta-5 desaturase steps that convert dietary essential fatty acids toward longer omega-6 products such as arachidonic acid. Human nutrition perspectives describe these desaturation steps as integral to omega-3 and omega-6 fatty acid biochemistry, meaning substrate selection helps determine which PUFA products accumulate.
Catalytic introduction of the omega-6 double bond
In simple terms: The enzyme removes hydrogens to create a new double bond at the omega-6 position.
The defining catalytic event of GO:0045485 is the introduction of an omega-6 double bond into the fatty acid hydrocarbon chain. This desaturation increases the number of double bonds in the acyl chain and changes the physical properties of the fatty acid. The desaturase hypothesis for atherosclerosis treats these desaturation reactions as central to omega-6 and omega-3 PUFA metabolism and to the balance of their downstream products. Because the reaction is enzymatic, its rate can vary between tissues and physiological states, as shown by measurements of delta-6 desaturase activity in rat liver microsomes.
Product formation and downstream PUFA flux
In simple terms: Once the double bond is added, the product can be elongated or used to make signaling lipids.
Products of omega-6 fatty acid desaturase activity feed into longer-chain omega-6 PUFAs, including arachidonic acid, which is a precursor for many lipid mediators. In human nutrition, the balance between omega-3 and omega-6 fatty acid biochemistry depends on these desaturation and elongation steps, so changes in desaturase activity can shift the entire PUFA profile. In activated macrophages, omega-3 and omega-6 fatty acids differentially impact cardiolipin remodeling, showing that the downstream products of these pathways have distinct membrane and signaling fates.
Tissue, age, and metabolic regulation of activity
In simple terms: The same enzyme can be more or less active depending on age, genetics, and metabolic state.
Delta-6 desaturase activity and fatty acid composition of rat liver microsomes are influenced by aging, indicating that GO:0045485 is not constant over the lifespan. In hereditary hypertriglyceridemic rats, delta-6 desaturase activity and gene expression are altered alongside glucose turnover rate, linking this activity to systemic metabolic phenotype. Human studies have related delta-5 and delta-6 desaturase activities to incident metabolic syndrome and serum zinc, suggesting that nutritional and trace-element status can modify the pathway. In human sebocytes, linoleic acid and arachidonic acid regulate delta-6 desaturase-2 expression and enhance proinflammatory activity without affecting lipogenesis, showing cell-type-specific regulation.
Pathophysiological consequences of altered activity
In simple terms: When this activity is too high or too low, it can contribute to disease processes.
The desaturase hypothesis for atherosclerosis proposes that these enzymes are Janus-faced in omega-6 and omega-3 PUFA metabolism, so altered activity may influence vascular disease risk. FADS1 contributes to anesthesia/surgery-induced cognitive impairment by aggravating omega-6 fatty acid metabolic disruption in aged mice, directly connecting this activity to a neurological phenotype. In human sebocytes, regulation of delta-6 desaturase-2 by linoleic acid and arachidonic acid leads to enhanced proinflammatory activity, providing a cellular mechanism for inflammatory skin biology.
Key Genes Involved in GO:0045485 omega-6 fatty acid desaturase activity
The genes most directly associated with GO:0045485 are the fatty acid desaturase genes FADS1 and FADS2, which encode the delta-5 and delta-6 desaturase steps of omega-6 PUFA metabolism [1,2].
| Gene | Major Role | Research Relevance |
|---|---|---|
| FADS2 | Delta-6 desaturase step in omega-6 PUFA metabolism [1,2] | Measured as delta-6 desaturase activity and gene expression in metabolic models |
| FADS1 | Delta-5 desaturase step in omega-6 PUFA metabolism [1,2] | Implicated in anesthesia/surgery-induced cognitive impairment via omega-6 metabolic disruption in aged mice |
| FADS2 (sebocyte context) | Delta-6 desaturase-2 expression regulated by linoleic and arachidonic acid | Links desaturase regulation to proinflammatory activity in human sebocytes |
| FADS1/FADS2 cluster | Desaturase hypothesis for atherosclerosis | Frames desaturases as Janus-faced enzymes in omega-6 and omega-3 PUFA metabolism |
| Delta-6 desaturase (rat liver) | Aging influence on activity and microsomal fatty acid composition | Model for age-related changes in desaturase activity |
| Delta-6 desaturase (hypertriglyceridemic rat) | Activity and gene expression linked to glucose turnover | Model for hereditary hypertriglyceridemia and metabolic dysregulation |
| Delta-5 desaturase (human) | Desaturase activity related to incident metabolic syndrome | Human observational marker of metabolic risk |
| Delta-6 desaturase (human) | Desaturase activity related to incident metabolic syndrome and serum zinc | Human observational marker of metabolic risk and nutrient interaction |
| Omega-6 PUFA products | Downstream fatty acids and lipid mediators | Readouts of desaturase pathway flux |
| Omega-3 PUFA pathway | Competing substrate context for desaturases [1,2] | Comparator for omega-6 versus omega-3 effects [1,2] |
| Cardiolipin remodeling machinery | Membrane lipid remodeling in activated macrophages | Readout of differential omega-3 and omega-6 impact |
| Arachidonic acid pathway | Product of omega-6 desaturation and precursor for signaling lipids | Links desaturase activity to inflammation |
| Linoleic acid substrate | Dietary essential fatty acid entering the desaturation pathway [1,2] | Substrate-level control of omega-6 desaturase flux [1,2] |
| FADS2 in sebocytes | Regulated by linoleic and arachidonic acid | Cell-type-specific inflammatory model |
| FADS1 in aged mouse brain | Aggravates omega-6 fatty acid metabolic disruption | Neurological model of perioperative cognitive impairment |
| Delta-6 desaturase in liver microsomes | Activity measured biochemically | Biochemical assay model for desaturase function |
How Is omega-6 fatty acid desaturase activity Regulated?
Omega-6 fatty acid desaturase activity is regulated at multiple levels. At the substrate level, linoleic acid and arachidonic acid regulate delta-6 desaturase-2 expression in human sebocytes, and this regulation enhances proinflammatory activity without affecting lipogenesis. At the physiological level, aging influences delta-6 desaturase activity and the fatty acid composition of rat liver microsomes. Genetic and metabolic background also matters: hereditary hypertriglyceridemic rats show altered delta-6 desaturase activity and gene expression together with changes in glucose turnover rate. In humans, delta-5 and delta-6 desaturase activities have been related to incident metabolic syndrome and serum zinc, suggesting that nutrient status may modify the pathway. The desaturase hypothesis for atherosclerosis further proposes that the balance between omega-6 and omega-3 PUFA metabolism is a key regulatory axis for disease risk.
omega-6 fatty acid desaturase activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| FADS1 | Anesthesia/surgery-induced cognitive impairment in aged mice | Aged mouse model with FADS1 manipulation and behavioral testing |
| FADS2 | Proinflammatory activity in human sebocytes | Human sebocyte cell culture with linoleic and arachidonic acid treatment |
| FADS1/FADS2 | Atherosclerosis via desaturase hypothesis | Lipid-loaded macrophage or vascular cell models with desaturase perturbation |
| Delta-6 desaturase | Hereditary hypertriglyceridemia and glucose turnover | Hereditary hypertriglyceridemic rat model |
| Delta-5/delta-6 desaturase | Incident metabolic syndrome and serum zinc | Human cohort observational study with desaturase activity estimates |
Atherosclerosis and cardiovascular risk
The desaturase hypothesis for atherosclerosis positions omega-6 and omega-3 desaturases as Janus-faced enzymes whose balance influences vascular disease. This hypothesis connects GO:0045485 to lipid-driven cardiovascular pathology and provides a rationale for measuring desaturase activity in cardiovascular research. Human nutrition perspectives on omega-3 and omega-6 fatty acid biochemistry support the idea that desaturation steps shape the fatty acid pools relevant to cardiovascular health.
Metabolic syndrome and glucose metabolism
Delta-5 and delta-6 desaturase activities have been studied in relation to incident metabolic syndrome and serum zinc in human cohorts. In hereditary hypertriglyceridemic rats, delta-6 desaturase activity and gene expression are altered alongside glucose turnover rate, linking the activity to systemic metabolic regulation. Together, these findings suggest that GO:0045485 is relevant to metabolic risk stratification and to models of dyslipidemia and insulin resistance.
Inflammation and macrophage lipid remodeling
Omega-3 and omega-6 fatty acids differentially impact cardiolipin remodeling in activated macrophages, indicating that the products of desaturase activity influence mitochondrial membrane lipid composition during inflammation. In human sebocytes, regulation of delta-6 desaturase-2 by linoleic acid and arachidonic acid enhances proinflammatory activity without affecting lipogenesis, providing a cell-type-specific link between GO:0045485 and inflammatory signaling.
Cognitive impairment in aged models
FADS1 contributes to anesthesia/surgery-induced cognitive impairment by aggravating omega-6 fatty acid metabolic disruption in aged mice. This study directly connects a gene encoding a desaturase step to a neurological phenotype, suggesting that GO:0045485 may be a mechanistic node in perioperative neurocognitive disorders. It also highlights aging as a context that modifies the consequences of altered omega-6 metabolism [3,4].
From omega-6 fatty acid desaturase activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of FADS2 alter omega-6 PUFA flux? | FADS2 knockout cell model with lipidomics readout |
| Does a specific FADS1 variant change desaturase activity? | FADS1 point-mutation knock-in cell model |
| Does FADS1 overexpression worsen omega-6 metabolic disruption? | FADS1 overexpression cell model in neuronal or hepatic cells |
| Where is FADS2 expressed and how does it respond to substrate? | Tagged knock-in of FADS2 with imaging and substrate treatment |
| Does desaturase activity change with age or metabolic state? | Primary cells or animal models comparing young and aged conditions [3,5] |
| Does desaturase perturbation alter inflammatory lipid mediators? | Macrophage or sebocyte models with omega-3/omega-6 treatment [7,8] |
How to Study the omega-6 fatty acid desaturase activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Microsomal desaturase assay | Enzymatic activity of delta-6 desaturase | Liver tissue from aging or metabolic models |
| Gene expression analysis | Transcript levels of desaturase genes [5,8] | Hypertriglyceridemic rats or sebocyte cultures [5,8] |
| Fatty acid profiling | Composition of fatty acid pools | Assessment of desaturase pathway flux |
| Lipidomics of cardiolipin | Membrane lipid remodeling | Activated macrophage studies with omega-3/omega-6 treatment |
| Behavioral testing in aged mice | Cognitive impairment phenotype | Anesthesia/surgery models with FADS1 manipulation |
| Inflammatory activity assay | Proinflammatory readouts in sebocytes | Substrate regulation of delta-6 desaturase-2 |
| Human cohort desaturase estimation | Associations with metabolic syndrome and zinc | Observational studies of metabolic risk |
| Glucose turnover measurement | Systemic glucose metabolism | Hereditary hypertriglyceridemic rat model |
Biochemical measurement of desaturase activity
Delta-6 desaturase activity can be measured directly in tissue preparations such as rat liver microsomes, where activity and fatty acid composition are assessed together. In hereditary hypertriglyceridemic rats, delta-6 desaturase activity and gene expression were measured alongside glucose turnover rate, showing how biochemical and physiological readouts can be combined. These approaches provide the functional anchor for GO:0045485 annotation.
Gene expression and transcript analysis
Delta-6 desaturase gene expression has been quantified in metabolic models, including hereditary hypertriglyceridemic rats. In human sebocytes, expression of delta-6 desaturase-2 is regulated by linoleic acid and arachidonic acid, making transcript measurement a useful readout of substrate-driven regulation. RNA-level analysis helps distinguish changes in enzyme abundance from changes in catalytic efficiency.
Lipidomics and fatty acid profiling
Fatty acid composition of rat liver microsomes changes with aging, and these profiles reflect the activity of desaturases. Cardiolipin remodeling in activated macrophages differs between omega-3 and omega-6 fatty acid treatments, providing a lipidomic readout of downstream pathway effects. Human nutrition perspectives emphasize that omega-3 and omega-6 fatty acid biochemistry is best interpreted through comprehensive fatty acid profiling.
Disease-relevant functional assays
In aged mice, FADS1-dependent omega-6 fatty acid metabolic disruption has been linked to anesthesia/surgery-induced cognitive impairment, requiring behavioral and biochemical endpoints. In human sebocytes, proinflammatory activity can be measured after regulation of delta-6 desaturase-2 by linoleic and arachidonic acid. These assays connect molecular function to organismal or cellular phenotypes.
How CRISPR Can Be Used to Study GO:0045485 omega-6 fatty acid desaturase activity
Knockout
CRISPR knockout of FADS1 or FADS2 can remove the enzymatic steps carrying GO:0045485, allowing researchers to test whether omega-6 PUFA flux, inflammatory lipid mediators, or metabolic phenotypes depend on these genes. Knockout models are particularly useful for validating causal claims suggested by human association studies of desaturase activity and metabolic syndrome or by the desaturase hypothesis for atherosclerosis.
Point Mutation
Point-mutation models can introduce specific amino acid changes into FADS1 or FADS2 to test how catalytic residues or regulatory sites affect omega-6 double-bond introduction. Such models help separate loss of enzyme abundance from loss of catalytic function, which is important when interpreting desaturase activity measurements in disease contexts [1,4].
Knock-in
Knock-in strategies can add tags or reporter sequences to endogenous FADS1 or FADS2, enabling tracking of expression and localization in relevant cell types. Tagged knock-in models are useful for studying substrate-regulated expression, as seen when linoleic acid and arachidonic acid regulate delta-6 desaturase-2 in human sebocytes.
Overexpression
Overexpression of FADS1 or FADS2 can drive excess omega-6 desaturase activity and test whether increased flux is sufficient to produce phenotypes such as enhanced proinflammatory activity or metabolic disruption. Overexpression models complement knockout studies by establishing sufficiency rather than necessity.
How EDITGENE Supports omega-6 fatty acid desaturase activity Research
Researchers studying omega-6 fatty acid desaturase activity-related genes often need to determine whether a candidate gene is causally involved in lipid metabolism, inflammation, or metabolic disease, rather than merely correlated with it. The published literature on FADS1, FADS2, and desaturase activity provides strong hypotheses [1,4,6,8], but causal testing requires precise genetic models. EDITGENE provides the CRISPR tools and cell models needed to move from association to mechanism.
Contact EDITGENE today to design your custom CRISPR model for omega-6 fatty acid desaturase activity research.
Frequently Asked Questions About omega-6 fatty acid desaturase activity
What is omega-6 fatty acid desaturase activity?
It is the catalytic activity defined by GO:0045485, which introduces an omega-6 double bond into a fatty acid hydrocarbon chain. It contributes to omega-6 PUFA metabolism and downstream products such as arachidonic acid.
What genes are involved in omega-6 fatty acid desaturase activity?
The main genes are FADS1 and FADS2, which encode delta-5 and delta-6 desaturase steps in omega-6 and omega-3 PUFA metabolism [1,2].
What is the GO ID for omega-6 fatty acid desaturase activity?
The GO ID is GO:0045485, and the ontology aspect is molecular_function.
How is omega-6 fatty acid desaturase activity measured?
It can be measured biochemically in tissue preparations such as rat liver microsomes and inferred from fatty acid profiles and desaturase gene expression [5,6].
Does omega-6 fatty acid desaturase activity change with age?
Yes, aging influences delta-6 desaturase activity and fatty acid composition of rat liver microsomes.
Is omega-6 fatty acid desaturase activity linked to metabolic syndrome?
Human studies have related delta-5 and delta-6 desaturase activities to incident metabolic syndrome and serum zinc.
How does omega-6 fatty acid desaturase activity affect inflammation?
In human sebocytes, regulation of delta-6 desaturase-2 by linoleic acid and arachidonic acid enhances proinflammatory activity without affecting lipogenesis. Omega-3 and omega-6 fatty acids also differentially impact cardiolipin remodeling in activated macrophages.
What diseases are associated with omega-6 fatty acid desaturase activity?
It has been linked to atherosclerosis through the desaturase hypothesis, metabolic syndrome, inflammatory skin biology, and anesthesia/surgery-induced cognitive impairment in aged mice.
Can CRISPR be used to study omega-6 fatty acid desaturase activity?
Yes, CRISPR knockout, point-mutation, knock-in, and overexpression models can test the causal role of FADS1, FADS2, and related genes in omega-6 PUFA metabolism.
Why is the desaturase hypothesis important for atherosclerosis?
It proposes that desaturases are Janus-faced enzymes in omega-6 and omega-3 PUFA metabolism, so their balance may influence vascular disease risk.
Conclusion
GO:0045485, omega-6 fatty acid desaturase activity, defines a central enzymatic step in omega-6 PUFA metabolism with broad relevance to cardiovascular, metabolic, inflammatory, and neurological research [1,4,6,8]. The literature shows that this activity is dynamic across age, genetic background, and nutritional state [3,5,6], and that its products influence membrane lipids and signaling [7,8]. For researchers, the next step is often causal testing with precise genetic models. By combining knockout, point-mutation, knock-in, overexpression, CRISPR library screening, and bioinformatics services, EDITGENE supports mechanistic studies of omega-6 fatty acid desaturase activity from hypothesis to publication-ready data.
References
- 1. Martinelli N et al.. 2009. A 'desaturase hypothesis' for atherosclerosis: Janus-faced enzymes in omega-6 and omega-3 polyunsaturated fatty acid metabolism.. J Nutrigenet Nutrigenomics 2(3):129-39 PMID: 19776640
- 2. Innis SM. 2014. Omega-3 fatty acid biochemistry: perspectives from human nutrition.. Mil Med 179(11 Suppl):82-7 PMID: 25373090
- 3. Bordoni A et al.. 1988. Aging influence on delta-6-desaturase activity and fatty acid composition of rat liver microsomes.. Biochem Int 17(6):1001-9 PMID: 3245835
- 4. Chen Z et al.. 2026. FADS1 contributes to anesthesia/surgery-induced cognitive impairment by aggravating omega-6 fatty acid metabolic disruption in aged mice.. J Neuroinflammation 23(1) PMID: 41673763
- 5. Demcakova E et al.. 2001. Delta-6 desaturase activity and gene expression, tissue fatty acid profile and glucose turnover rate in hereditary hypertriglyceridemic rats.. Endocr Regul 35(4):179-86 PMID: 11858764
- 6. Yary T et al.. 2017. Omega-6 polyunsaturated fatty acids, serum zinc, delta-5- and delta-6-desaturase activities and incident metabolic syndrome.. J Hum Nutr Diet 30(4):506-514 PMID: 28699199
- 7. Chang WH et al.. 2018. Omega-3 and omega-6 fatty acid differentially impact cardiolipin remodeling in activated macrophage.. Lipids Health Dis 17(1):201 PMID: 30153842
- 8. Zouboulis CC et al.. 2011. Regulation of stearoyl-coenzyme A desaturase and fatty acid delta-6 desaturase-2 expression by linoleic acid and arachidonic acid in human sebocytes leads to enhancement of proinflammatory activity but does not affect lipogenesis.. Br J Dermatol 165(2):269-76 PMID: 21457203
