What you carry at this position in your DNA and what research says about it.
Fatty Acid Metabolism: 6/10 evidence, 14 publications.
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Sample genotype (not yours): G/G
Higher Inflammatory Fatty Acids and Blood Glucose
Highly efficient fatty acid conversion leads to higher levels of arachidonic acid, which can raise cardiovascular inflammation and blood glucose. Triglyceride levels tend to run lower.
What this genotype means: Higher blood triglyceride levels; Elevated blood glucose levels; Increased inflammatory fatty acid conversion.
Sample genotype (not yours): A/A
Lower Inflammatory Fatty Acids and Blood Glucose
Slower fatty acid conversion results in lower levels of inflammatory arachidonic acid and blood glucose, which is generally protective, though triglyceride levels tend to run slightly higher.
What this genotype means: Lower blood triglyceride levels; Reduced inflammatory fatty acid levels; Slower conversion of plant-based omega fatty acids.
Sample genotype (not yours): G/A
Typical Fatty Acid and Lipid Levels
A balanced, intermediate rate of fatty acid conversion keeps triglyceride and blood glucose levels within the typical average range.
What this genotype means: Balanced fatty acid conversion; Typical blood triglyceride levels; Standard blood glucose levels.
Gene function and biological role
Gene Function: TMEM258 plays a critical role in cellular homeostasis and lipid metabolism. It is situated in a highly active gene cluster alongside FADS1 and FADS2, which encode key desaturase enzymes [1]. These desaturase enzymes are responsible for converting short-chain dietary fatty acids into long-chain polyunsaturated fatty acids like arachidonic acid, EPA, and DHA [2]. TMEM258 itself is involved in endoplasmic reticulum stress and inflammatory responses, particularly in the gut [3]. Genetic variations in this region are among the strongest known determinants of circulating lipid and fatty acid levels in humans [4].
Variant Impact: Located upstream of TMEM258, the rs174538 variant is in tight linkage disequilibrium with functional variants that directly control the expression of desaturase enzymes [1]. The G allele represents the highly active ancestral version, which promotes rapid conversion of plant-derived fatty acids into highly active long-chain fatty acids [2]. Conversely, the A allele reduces desaturase activity, leading to a slower conversion rate and lower levels of circulating arachidonic acid [3]. Because of this profound effect on lipid synthesis, rs174538 is strongly associated with blood triglyceride levels, glucose levels, and inflammatory markers [5].
Key Insight: This variant acts as a genetic dial for how efficiently your body converts plant-based omega fatty acids into highly active, potentially inflammatory forms.
Location: TMEM258. Chromosome 11 · 11q12.2 · 61.8 Mb
Origin Story: Strong positive selection in agricultural populations favored alleles that increase desaturase activity, allowing efficient synthesis of long-chain polyunsaturated fatty acids from vegetarian diets.
Estimated prevalence by population
Global 56.4%; European 48.4%; African 86.4%; East Asian 20.4%; South Asian 70.1%; Americas 28.2%; Ashkenazi 56.6%; Finnish 43.3%; Middle Eastern 47.7%; Amish 62.2%.
Estimated GG genotype frequency.
Global 34.8%; European 42.3%; African 13.1%; East Asian 49.5%; South Asian 27.2%; Americas 49.8%; Ashkenazi 37.2%; Finnish 45.0%; Middle Eastern 42.7%; Amish 33.4%.
Estimated GA genotype frequency.
Global 8.7%; European 9.2%; African 0.5%; East Asian 30.1%; South Asian 2.6%; Americas 22.0%; Ashkenazi 6.1%; Finnish 11.7%; Middle Eastern 9.6%; Amish 4.5%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Nutrition & Metabolism
Macronutrient Metabolism
Fatty Acid Conversion. Evidence: 6/10. Source: PMID 31991592. Highly Efficient.
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 6/10. Source: PMID 34503513. Decreased Levels.
Diabetes & Glycemic Traits
Blood Glucose. Evidence: 6/10. Source: PMID 36333282. Increased Levels.
Gout & Uric Acid
Uric Acid Levels. Evidence: 6/10. Source: PMID 39789286. Decreased Levels.
Showing effects for A/A genotype
Fatty Acid Conversion. Evidence: 6/10. Source: PMID 31991592. Slower Conversion.
Triglycerides. Evidence: 6/10. Source: PMID 34503513. Increased Levels.
Blood Glucose. Evidence: 6/10. Source: PMID 36333282. Decreased Levels.
Uric Acid Levels. Evidence: 6/10. Source: PMID 39789286. Increased Levels.
Showing effects for G/A genotype
Fatty Acid Conversion. Evidence: 6/10. Source: PMID 31991592. Moderate.
Triglycerides. Evidence: 6/10. Source: PMID 34503513. Typical Levels.
Blood Glucose. Evidence: 6/10. Source: PMID 36333282. Typical Levels.
Uric Acid Levels. Evidence: 6/10. Source: PMID 39789286. Typical Levels.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Two copies of the G allele result in maximum activity of the desaturase enzymes in the FADS cluster [1]. This highly efficient pathway rapidly converts plant-based omega-3 and omega-6 precursors into highly active long-chain fatty acids like arachidonic acid [2]. While this ensures a robust supply of essential lipids, arachidonic acid is also a primary precursor for pro-inflammatory signaling molecules [3]. Consequently, this genotype is linked to higher blood glucose levels and greater inflammatory activity, though it is associated with lower circulating triglycerides [4]. It may also correlate with increased severity of inflammatory conditions such as Crohn's disease [1]. Managing dietary saturated fat and balancing omega-6 with omega-3 fatty acids can help mitigate these risks.
Higher blood triglyceride levels; Elevated blood glucose levels; Increased inflammatory fatty acid conversion.
Sample genotype: AA (Homozygous)
Two copies of the A allele significantly reduce the activity of the desaturase enzymes in the FADS cluster [1]. This slower conversion rate leads to lower circulating levels of arachidonic acid, which in turn reduces the production of pro-inflammatory signaling molecules [2]. As a result, this genotype is associated with lower blood glucose levels and reduced inflammatory activity, although circulating triglycerides tend to run slightly higher [3]. The lower inflammatory profile is generally favorable, but because the conversion of plant-based omega-3s to active EPA and DHA is less efficient, direct dietary intake of marine-derived omega-3s may be beneficial [4]. It is also linked to slightly higher urate levels, a minor trade-off to monitor [3].
Lower blood triglyceride levels; Reduced inflammatory fatty acid levels; Slower conversion of plant-based omega fatty acids.
Sample genotype: GA (Heterozygous)
One G allele paired with one A allele results in moderate desaturase enzyme activity [1]. This intermediate state provides a balanced conversion rate of dietary plant-based fatty acids into active long-chain lipids [2]. Levels of arachidonic acid and other highly active lipids are typically stable and do not reach the elevated levels seen in G/G carriers [3]. Similarly, blood triglycerides and glucose levels generally remain within the standard population average [4]. There is no significantly elevated risk for lipid-driven cardiovascular inflammation or severe desaturase-related metabolic imbalances. Maintaining a standard healthy diet rich in diverse fatty acids supports optimal metabolic function.
Balanced fatty acid conversion; Typical blood triglyceride levels; Standard blood glucose levels.
Variants with shared genetic architecture
rs102275 · TMEM258 Gene · Chr 11 · Cholesterol and Crohn's Risk
rs740006 · TMEM258 Gene · Chr 11 · Blood Lipid Balance
rs174568 · FADS2 Gene · Chr 11 · Omega Fatty Acid Conversion
Whole-Genome Sequencing Analysis of Human Metabolome in Multi-Ethnic Populations.
Content updated August 2026.
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