What you carry at this position in your DNA and what research says about it.
Triglyceride and Liver Health: 9/10 evidence, 13 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): C/C
Typical Triglyceride Levels and Standard Metabolic Profile
Carrying two copies of the common C allele is associated with typical triglyceride levels and standard liver enzyme activity. This profile represents the baseline metabolic risk in the general population.
What this genotype means: Typical triglyceride levels; Standard liver enzyme activity.
Sample genotype (not yours): C/T
Slightly Lower Triglycerides and Favorable Metabolic Profile
Carrying one copy of the protective T allele is linked to slightly lower triglyceride levels and improved liver enzyme markers. This profile offers a mild protective effect against metabolic stress.
What this genotype means: Slightly lower triglycerides; Slightly lower liver enzymes.
Sample genotype (not yours): T/T
Lower Triglycerides and Protective Metabolic Profile
Two copies of the protective T allele are linked to lower triglyceride levels and higher HDL cholesterol. This profile is also associated with lower liver enzymes and reduced uric acid.
What this genotype means: Lower triglyceride levels; Lower liver enzyme markers; Reduced risk of gout.
Gene function and biological role
Gene Function: The MLXIPL gene encodes the carbohydrate response element-binding protein, a major transcription factor that controls how the liver processes sugars and fats [1]. When glucose levels rise, this protein activates genes involved in lipogenesis, the pathway that converts excess carbohydrates into triglycerides [1]. This regulation is crucial for maintaining systemic energy balance and lipid homeostasis [2]. Variations in this gene can alter its transcriptional activity, directly impacting circulating lipid profiles and liver fat accumulation [2]. Consequently, MLXIPL is a key player in metabolic syndrome, fatty liver disease, and cardiovascular risk [1] [2].
Variant Impact: Located in an intron of the MLXIPL gene, rs17145750 is a common single nucleotide variant that influences the expression and activity of the carbohydrate response element-binding protein [1]. The C allele is associated with higher expression of lipogenic genes, leading to increased synthesis of triglycerides and higher levels of liver enzymes [2]. Conversely, the T allele appears to reduce this lipogenic drive, resulting in a more favorable metabolic profile [1]. This genetic change has wide-ranging effects on blood lipids, liver function markers, and uric acid levels [2] [3]. Understanding this variant helps clarify individual differences in metabolic efficiency and susceptibility to lipid-related disorders [1] [3].
Key Insight: This variant acts as a metabolic coordinator, simultaneously influencing blood triglycerides, liver enzymes, and uric acid levels through a single genetic pathway.
Location: MLXIPL. Chromosome 7 · 7q11.23 · 73.6 Mb
Estimated prevalence by population
Global 75.2%; European 71.2%; African 79.3%; East Asian 79.0%; South Asian 82.3%; Americas 80.6%; Ashkenazi 71.8%; Finnish 74.3%; Middle Eastern 74.8%; Amish 72.3%.
Estimated CC genotype frequency.
Global 22.9%; European 26.4%; African 19.5%; East Asian 19.8%; South Asian 16.8%; Americas 18.3%; Ashkenazi 25.8%; Finnish 23.8%; Middle Eastern 23.4%; Amish 25.4%.
Estimated CT genotype frequency.
Global 1.8%; European 2.4%; African 1.2%; East Asian 1.2%; South Asian 0.9%; Americas 1.0%; Ashkenazi 2.3%; Finnish 1.9%; Middle Eastern 1.8%; Amish 2.2%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 9/10. Source: PMID 21726544. Typical.
Gout & Uric Acid
Uric Acid Levels. Evidence: 8/10. Source: PMID 30993211. Typical.
Organ Systems
Liver Function & Disease
GGT Liver Enzyme. Evidence: 8/10. Source: PMID 22001757. Typical.
Alkaline Phosphatase. Evidence: 8/10. Source: PMID 33547301. Typical.
Showing effects for C/T genotype
Triglycerides. Evidence: 9/10. Source: PMID 21726544. Lower.
Uric Acid Levels. Evidence: 8/10. Source: PMID 30993211. Lower.
GGT Liver Enzyme. Evidence: 8/10. Source: PMID 22001757. Lower.
Alkaline Phosphatase. Evidence: 8/10. Source: PMID 33547301. Lower.
Showing effects for T/T genotype
Triglycerides. Evidence: 9/10. Source: PMID 21726544. Lowest.
Uric Acid Levels. Evidence: 8/10. Source: PMID 30993211. Lowest.
GGT Liver Enzyme. Evidence: 8/10. Source: PMID 22001757. Lowest.
Alkaline Phosphatase. Evidence: 8/10. Source: PMID 33547301. Lowest.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Carrying two copies of the C allele is associated with standard activity of the ChREBP transcription factor, promoting typical hepatic lipogenesis [1]. This metabolic state leads to standard circulating levels of triglycerides and typical HDL cholesterol [1]. Additionally, studies show a baseline association with standard liver enzymes, specifically gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP), which are markers of liver function [2]. Uric acid levels also tend to be typical in those with this genotype, representing a standard risk for gout [3]. These combined metabolic factors contribute to a baseline risk for cardiovascular disease and metabolic syndrome [1] [2].
Typical triglyceride levels; Standard liver enzyme activity.
Sample genotype: CT (Heterozygous)
Possessing one C allele and one T allele generally results in a favorable metabolic profile that is slightly improved compared to the population average [1]. Triglyceride levels tend to be lower, while HDL cholesterol levels may be slightly higher, as the protective T allele reduces hepatic fat synthesis [1]. Liver enzyme levels, including GGT and ALP, are often slightly lower, indicating efficient liver metabolic function and reduced fat accumulation [2]. Uric acid levels also remain slightly below baseline, presenting a reduced risk for gout development [3]. This balanced state means that lifestyle factors, such as diet and exercise, can easily build upon this genetic advantage to support optimal metabolic health [1] [2]. Maintaining a balanced diet low in refined sugars further supports healthy lipid levels [1]. Standard cardiovascular and liver health guidelines are highly effective for this genotype [2].
Slightly lower triglycerides; Slightly lower liver enzymes.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele is associated with reduced activity of the ChREBP pathway, leading to lower rates of hepatic fat synthesis [1]. This genetic profile is highly favorable, characterized by lower circulating triglycerides and higher HDL cholesterol levels [1]. Liver enzyme levels, such as GGT and ALP, are typically lower, suggesting a reduced risk of liver fat accumulation and stress [2]. Furthermore, uric acid levels are significantly lower, which provides a protective effect against the development of gout [3]. These combined factors contribute to a lower overall risk of cardiovascular disease and metabolic syndrome [1] [2]. Individuals with this genotype may process dietary carbohydrates more efficiently, with less tendency to store them as fat [1]. Emphasizing a whole-foods diet can further enhance this naturally protective metabolic advantage [1] [2].
Lower triglyceride levels; Lower liver enzyme markers; Reduced risk of gout.
Variants with shared genetic architecture
rs3812316 · MLXIPL Gene · Chr 7 · Triglyceride Levels
rs55747707 · MLXIPL Gene · Chr 7 · Cholesterol and Lipids
rs34060476 · MLXIPL Gene · Chr 7 · Triglyceride Levels
Genome-wide association study identifies loci influencing concentrations of liver enzymes in plasma.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com