What you carry at this position in your DNA and what research says about it.
Triglyceride Levels: 10/10 evidence, 32 publications.
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Sample genotype (not yours): T/T
Higher Triglycerides and Gout Risk
Elevated triglyceride levels and higher blood uric acid are characteristic of this genetic profile. It also increases the risk of developing kidney stones and Crohn's disease, though it offers a slight protective effect against type 2 diabetes.
What this genotype means: Significantly higher triglyceride levels; Increased risk of gout and kidney stones; Slightly lower risk of type 2 diabetes.
Sample genotype (not yours): C/C
Lower Triglycerides and Gout Risk
Lower levels of triglycerides, cholesterol, and uric acid characterize this genetic profile, reducing the risk of gout and kidney stones. However, it carries a slightly higher risk of type 2 diabetes.
What this genotype means: Lower triglyceride and cholesterol levels; Reduced risk of gout and kidney stones; Slightly higher risk of type 2 diabetes.
Sample genotype (not yours): T/C
Typical Triglyceride and Gout Risk
Possessing one copy of each allele results in intermediate metabolic effects. Triglyceride, cholesterol, and uric acid levels are typically near the population average.
What this genotype means: Typical blood lipid profile; Average risk of gout and kidney stones; Standard risk of type 2 diabetes.
Gene function and biological role
Gene Function: GCKR encodes the glucokinase regulatory protein, which regulates the activity of glucokinase in the liver and pancreatic beta cells [1]. Glucokinase is a key enzyme that acts as a sensor for blood glucose levels and controls glucose storage and utilization [1]. The regulatory protein binds to glucokinase to inhibit its activity when glucose levels are low, releasing it when glucose levels rise [1]. Variations in this gene can alter this regulatory balance, shifting how the liver processes carbohydrates and fats [2]. This shift has a direct impact on circulating blood lipids, uric acid levels, and insulin sensitivity [3].
Variant Impact: Located in an intron of the GCKR gene, rs780093 is a common single nucleotide polymorphism [4]. Although it does not directly change the amino acid sequence of the protein, it is in strong linkage disequilibrium with functional variants that alter regulatory protein activity [4]. The change affects how tightly the regulatory protein binds to glucokinase, thereby modifying hepatic glucose uptake and fat synthesis [1]. This genetic variation leads to a distinct metabolic trade-off between blood lipid levels and glucose regulation [3].
Key Insight: This variant creates a direct metabolic trade-off where the allele that protects against high triglycerides and gout actually increases the risk of type 2 diabetes.
Location: GCKR. Chromosome 2 · 2p23.3 · 27.5 Mb
Estimated prevalence by population
Global 12.1%; European 16.1%; African 2.1%; East Asian 24.3%; South Asian 5.5%; Americas 14.3%; Ashkenazi 29.1%; Finnish 13.2%; Middle Eastern 24.3%; Amish 8.5%.
Estimated TT genotype frequency.
Global 41.0%; European 48.1%; African 24.6%; East Asian 50.0%; South Asian 35.9%; Americas 47.0%; Ashkenazi 49.7%; Finnish 46.3%; Middle Eastern 50.0%; Amish 41.3%.
Estimated TC genotype frequency.
Global 46.9%; European 35.8%; African 73.4%; East Asian 25.8%; South Asian 58.6%; Americas 38.7%; Ashkenazi 21.2%; Finnish 40.5%; Middle Eastern 25.7%; Amish 50.2%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 10/10. Source: PMID 21386085. Elevated Levels.
Gout & Uric Acid
Uric Acid Levels. Evidence: 6/10. Source: PMID 20884846. Elevated Levels.
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 4/10. Source: PMID 26818947. Lowered Risk.
Organ Systems
Kidney Function & Disease
Kidney Stones. Evidence: 6/10. Source: PMID 31729369. ~1.1x Higher Risk.
Immunity & Inflammation
Chronic Inflammatory Diseases
Crohn's Disease. Evidence: 5/10. Source: PMID 21102463. ~1.15x Higher Risk.
Showing effects for C/C genotype
Triglycerides. Evidence: 10/10. Source: PMID 21386085. Lowered Levels.
Uric Acid Levels. Evidence: 6/10. Source: PMID 20884846. Lowered Levels.
Type 2 Diabetes. Evidence: 4/10. Source: PMID 26818947. ~1.08x Higher Risk.
Kidney Stones. Evidence: 6/10. Source: PMID 31729369. Lowered Risk.
Crohn's Disease. Evidence: 5/10. Source: PMID 21102463. Lowered Risk.
Showing effects for T/C genotype
Triglycerides. Evidence: 10/10. Source: PMID 21386085. Typical Levels.
Uric Acid Levels. Evidence: 6/10. Source: PMID 20884846. Typical Levels.
Type 2 Diabetes. Evidence: 4/10. Source: PMID 26818947. Typical Risk.
Kidney Stones. Evidence: 6/10. Source: PMID 31729369. Typical Risk.
Crohn's Disease. Evidence: 5/10. Source: PMID 21102463. Typical Risk.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Two copies of the T allele are linked to a notable increase in circulating triglycerides and very low-density lipoprotein (VLDL) cholesterol [1]. This occurs because the T allele is associated with enhanced hepatic glucokinase activity, which drives the liver to convert more glucose into fats [1]. Consequently, total and LDL cholesterol levels are often higher [2]. Additionally, this metabolic shift reduces the excretion of uric acid, leading to higher blood urate levels and an increased risk of gout [3]. The elevated urate also contributes to a higher likelihood of developing kidney stones [4]. Interestingly, because the liver is highly active in processing glucose under this genotype, fasting blood glucose levels tend to be lower, which slightly reduces the risk of type 2 diabetes [5].
Significantly higher triglyceride levels; Increased risk of gout and kidney stones; Slightly lower risk of type 2 diabetes.
Sample genotype: CC (Homozygous)
Two copies of the C allele are highly beneficial for cardiovascular and joint health, as they are linked to significantly lower triglyceride levels [1]. This genotype is associated with reduced total cholesterol, LDL cholesterol, and VLDL cholesterol, promoting a healthier lipid profile [2]. Furthermore, blood uric acid levels are lower, which substantially decreases the risk of developing gout [3]. The lower urate levels also translate to a reduced risk of kidney stones [4]. However, because this variant slightly reduces hepatic glucose uptake, fasting blood glucose levels can be slightly higher, leading to a modest increase in the risk of type 2 diabetes [5]. Despite this minor diabetes caveat, the overall metabolic profile is highly protective against dyslipidemia and gout.
Lower triglyceride and cholesterol levels; Reduced risk of gout and kidney stones; Slightly higher risk of type 2 diabetes.
Sample genotype: TC (Heterozygous)
A balanced metabolic profile is typical for those with one T allele and one C allele. This heterozygous state generally results in average levels of circulating triglycerides and cholesterol [1]. Uric acid levels and the associated risk of gout are also typical, falling between the higher-risk T/T genotype and the lower-risk C/C genotype [2]. The risk of developing kidney stones or Crohn's disease remains close to the baseline population rate [3] [4]. Similarly, the likelihood of developing type 2 diabetes is not significantly altered, as the protective effect of the T allele is balanced by the C allele [5]. Overall, this genotype represents a standard metabolic profile without extreme genetic predispositions in either direction.
Typical blood lipid profile; Average risk of gout and kidney stones; Standard risk of type 2 diabetes.
Variants with shared genetic architecture
rs1260326 · GCKR Gene · Chr 2 · Metabolic Health
rs780094 · GCKR Gene · Chr 2 · Metabolic Health
rs1260333 · GCKR Gene · Chr 2 · Triglyceride Levels
Genome-wide association study of metabolic syndrome in Korean populations.
A large electronic-health-record-based genome-wide study of serum lipids.
Genetic variants of calcium and vitamin D metabolism in kidney stone disease.
Content updated August 2026.
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