What you carry at this position in your DNA and what research says about it.
Triglyceride Levels: 10/10 evidence, 25 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 Triglycerides and Baseline Gout Risk
Carrying two copies of the common C allele results in typical levels of blood fats and a standard risk of developing gout. Liver enzyme levels and fat accumulation in the liver are also at baseline levels.
What this genotype means: Typical blood triglyceride levels; Standard baseline risk of gout; Normal liver fat clearance.
Sample genotype (not yours): C/G
Lower Triglycerides and Reduced Gout Risk
Possessing one copy of the G allele is associated with lower circulating blood triglycerides and a reduced risk of gout. There is only a very minor, typical risk of fat accumulation in the liver.
What this genotype means: Lower circulating blood triglycerides; Reduced risk of developing gout; Slightly higher HDL cholesterol.
Sample genotype (not yours): G/G
Lowest Triglycerides but Higher Liver Fat Risk
Carrying two copies of the G allele represents a metabolic trade-off, offering the lowest blood triglycerides alongside an increased risk of fat buildup in the liver.
What this genotype means: Lowest blood triglyceride levels; Strong protection against gout; Increased risk of fat accumulation in the liver.
Gene function and biological role
Gene Function: The MLXIPL gene encodes the carbohydrate-responsive element-binding protein, also known as ChREBP [1]. This transcription factor plays a central role in regulating de novo lipogenesis, the process by which the liver converts excess carbohydrates into fatty acids [2]. In response to glucose, ChREBP activates the expression of key enzymes involved in glycolysis and lipid synthesis [2]. Consequently, variations in this gene can significantly alter how the body processes dietary sugars and packages them into fats [1].
Variant Impact: Changing the amino acid glutamine to histidine at position 241 (p.Gln241His), the rs3812316 variant alters a highly conserved region of the MLXIPL protein [1]. This specific modification occurs in a domain that is critical for the activation of the ChREBP transcription factor [2]. The variant G allele produces a less stable version of the protein, which reduces its overall transcriptional activity [2]. As a result, individuals carrying the G allele experience decreased fat synthesis in response to carbohydrates, leading to lower circulating blood fats [1].
Key Insight: The G allele acts as a natural brake on fat synthesis, lowering blood triglycerides but potentially causing fat to build up in the liver instead.
Location: MLXIPL. Chromosome 7 · 7q11.23 · 73.6 Mb
Origin Story: Because MLXIPL coordinates energy storage from carbohydrates, it has been proposed as a classic thrifty gene that helped ancient humans survive periods of famine by efficiently storing fat.
Estimated prevalence by population
Global 82.1%; European 76.2%; African 91.5%; East Asian 82.3%; South Asian 83.1%; Americas 86.3%; Ashkenazi 78.8%; Finnish 77.6%; Middle Eastern 76.9%; Amish 83.6%.
Estimated CC genotype frequency.
Global 16.9%; European 22.2%; African 8.3%; East Asian 16.9%; South Asian 16.1%; Americas 13.2%; Ashkenazi 19.9%; Finnish 21.0%; Middle Eastern 21.6%; Amish 15.6%.
Estimated CG genotype frequency.
Global 1.0%; European 1.6%; African 0.2%; East Asian 0.9%; South Asian 0.8%; Americas 0.5%; Ashkenazi 1.3%; Finnish 1.4%; Middle Eastern 1.5%; Amish 0.7%.
Estimated GG genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 10/10. Source: PMID 18193046. Typical.
HDL Cholesterol. Evidence: 10/10. Source: PMID 35213538. Typical.
Gout & Uric Acid
Gout. Evidence: 10/10. Source: PMID 36281732. Typical Risk.
Organ Systems
Liver Function & Disease
Fatty Liver Disease. Evidence: 10/10. Source: PMID 38632349. Typical Risk.
Showing effects for C/G genotype
Triglycerides. Evidence: 10/10. Source: PMID 18193046. ~10% Lower.
HDL Cholesterol. Evidence: 10/10. Source: PMID 35213538. Slightly Higher.
Gout. Evidence: 10/10. Source: PMID 36281732. Lower Risk.
Showing effects for G/G genotype
Triglycerides. Evidence: 10/10. Source: PMID 18193046. ~20% Lower.
HDL Cholesterol. Evidence: 10/10. Source: PMID 35213538. Higher.
Gout. Evidence: 10/10. Source: PMID 36281732. Lowest Risk.
Fatty Liver Disease. Evidence: 10/10. Source: PMID 38632349. Higher Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Fasting blood triglycerides and cholesterol levels are expected to be within the normal range for the general population [1]. Because the common C allele encodes a fully active version of the ChREBP protein, dietary carbohydrates are efficiently converted into fats and released into the bloodstream [2]. While this process is highly efficient, it can lead to elevated blood triglycerides if dietary sugar intake is consistently high [1]. The risk of developing gout is also at the standard population baseline [3]. On the positive side, there is no elevated genetic risk for fat accumulation in the liver or elevated liver enzymes [4]. Maintaining a balanced diet low in refined sugars remains the most effective way to keep blood fats in a healthy range. Regular cardiovascular exercise also helps support optimal lipid metabolism.
Typical blood triglyceride levels; Standard baseline risk of gout; Normal liver fat clearance.
Sample genotype: CG (Heterozygous)
Circulating blood triglycerides are significantly lower than the population average due to reduced activity of the fat-producing ChREBP protein [1]. This reduction in blood fats also translates to a lower likelihood of developing gout, a painful joint condition linked to metabolic markers [2]. Because only one copy of the G allele is present, the liver still maintains sufficient capacity to export fats, keeping liver enzyme levels stable [3]. High-density lipoprotein (HDL) cholesterol levels also tend to be slightly higher, which is beneficial for cardiovascular health [4]. This combination offers a favorable metabolic profile with minimal trade-offs. Emphasizing a Mediterranean-style diet can further optimize these natural metabolic advantages [5]. Limiting simple sugars helps maintain this healthy balance without straining the liver.
Lower circulating blood triglycerides; Reduced risk of developing gout; Slightly higher HDL cholesterol.
Sample genotype: GG (Homozygous)
Blood triglyceride levels are exceptionally low because the liver produces a highly unstable version of the ChREBP protein that limits fat synthesis [1]. This dramatic reduction in circulating blood fats provides strong protection against gout and supports healthy cardiovascular markers [2]. However, because the liver cannot efficiently package and export these fats into the bloodstream, lipids can accumulate within liver cells instead [3]. This accumulation can lead to elevated alanine aminotransferase (ALT) levels, a key marker of liver stress [4]. Over time, this increases the susceptibility to steatotic liver disease, particularly when combined with a high-sugar diet [3]. Managing dietary carbohydrate intake is crucial to prevent liver fat buildup while enjoying the cardiovascular benefits of low blood triglycerides. Avoiding excessive alcohol and monitoring liver enzymes during routine checkups are highly recommended strategies.
Lowest blood triglyceride levels; Strong protection against gout; Increased risk of fat accumulation in the liver.
Variants with shared genetic architecture
rs55747707 · MLXIPL Gene · Chr 7 · Cholesterol and Lipids
rs17145750 · MLXIPL Gene · Chr 7 · Triglyceride and Liver Health
rs34060476 · MLXIPL Gene · Chr 7 · Triglyceride Levels
Genome-wide scan identifies variation in MLXIPL associated with plasma triglycerides.
Metabolic and cardiovascular traits: an abundance of recently identified common genetic variants.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
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