What you carry at this position in your DNA and what research says about it.
Triglyceride Levels: 10/10 evidence, 27 publications.
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Sample genotype (not yours): C/C
Typical Triglyceride and Cholesterol Levels
Fasting triglyceride levels and HDL cholesterol are likely to be in the typical range. There is no genetically lowered risk for lipid-related metabolic conditions from this specific marker.
What this genotype means: Typical fasting triglyceride levels; Typical HDL cholesterol levels; Standard baseline risk for hypertriglyceridemia.
Sample genotype (not yours): C/T
Lower Triglycerides and Higher HDL Cholesterol
Fasting triglyceride levels are likely to be lower, while HDL cholesterol is slightly higher. This combination supports a more favorable cardiovascular and metabolic profile.
What this genotype means: Lower fasting triglyceride levels; Slightly higher HDL cholesterol levels; Reduced risk of hypertriglyceridemia.
Sample genotype (not yours): T/T
Lowest Triglycerides and Highest HDL Cholesterol
Fasting triglyceride levels are likely to be at their lowest, while HDL cholesterol is at its highest. This genotype offers the strongest genetic protection against high triglycerides.
What this genotype means: Lowest fasting triglyceride levels; Highest HDL cholesterol levels; Strong protection against hypertriglyceridemia.
Gene function and biological role
Gene Function: The TBL2 gene, or transducin beta like 2, is located on chromosome 7 in a region closely linked to lipid metabolism [1]. It resides adjacent to the MLXIPL gene, which encodes a key transcription factor regulating how the liver processes carbohydrates into fats [2]. While TBL2 itself is less understood, genetic variations in this genomic neighborhood strongly influence circulating blood lipids [3]. Research suggests that proteins in this region coordinate the expression of lipogenic enzymes in response to glucose levels [4]. Consequently, variations here are major determinants of cardiovascular and metabolic health markers [5].
Variant Impact: The rs17145738 variant is a single nucleotide polymorphism located in the 3 prime untranslated region of the TBL2 gene [1]. This genetic change is in high linkage disequilibrium with functional variants in the neighboring MLXIPL gene, meaning they are almost always inherited together [6]. Because of this close genetic link, rs17145738 serves as a highly reliable marker for how efficiently the body clears triglycerides [2]. Favorable metabolic profiles, including lower fasting triglycerides and higher HDL cholesterol, are consistently associated with the minor T allele [3]. Conversely, the more common C allele is linked to higher baseline triglycerides and an increased susceptibility to metabolic imbalances [5].
Key Insight: This variant is in such tight linkage with the MLXIPL gene that it acts as a perfect proxy for a functional mutation that alters how the liver converts dietary carbohydrates directly into fat.
Location: TBL2. Chromosome 7 · 7q11.23 · 73.6 Mb
Origin Story: The high prevalence of the protective lipid-lowering allele in certain Central Asian populations, such as Mongolians and Tibetans, suggests historical evolutionary selection to help nomadic pastoralists adapt to high-fat, high-protein livestock diets.
Estimated prevalence by population
Global 80.1%; European 77.1%; African 83.4%; East Asian 81.1%; South Asian 83.1%; Americas 85.2%; Ashkenazi 79.2%; Finnish 77.6%; Middle Eastern 76.4%; Amish 87.3%.
Estimated CC genotype frequency.
Global 18.7%; European 21.4%; African 15.9%; East Asian 17.9%; South Asian 16.1%; Americas 14.2%; Ashkenazi 19.6%; Finnish 21.0%; Middle Eastern 22.0%; Amish 12.3%.
Estimated CT genotype frequency.
Global 1.1%; European 1.5%; African 0.8%; East Asian 1.0%; South Asian 0.8%; Americas 0.6%; Ashkenazi 1.2%; Finnish 1.4%; Middle Eastern 1.6%; Amish 0.4%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 10/10. Source: PMID 18193043. Typical Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 20686565. Typical Levels.
Hypertriglyceridemia. Evidence: 4/10. Source: PMID 27599772. Typical Risk.
LDL Cholesterol. Evidence: 10/10. Source: PMID 29403010. Typical Levels.
Gout & Uric Acid
Uric Acid Levels. Evidence: 6/10. Source: PMID 31578528. Typical Levels.
Showing effects for C/T genotype
Triglycerides. Evidence: 10/10. Source: PMID 18193043. Lower Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 20686565. Higher Levels.
Hypertriglyceridemia. Evidence: 4/10. Source: PMID 27599772. Lower Risk.
Uric Acid Levels. Evidence: 6/10. Source: PMID 31578528. Lower Levels.
Showing effects for T/T genotype
Triglycerides. Evidence: 10/10. Source: PMID 18193043. Lowest Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 20686565. Highest Levels.
Hypertriglyceridemia. Evidence: 4/10. Source: PMID 27599772. Lowest Risk.
Uric Acid Levels. Evidence: 6/10. Source: PMID 31578528. Lowest Levels.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Fasting plasma triglyceride levels tend to remain at standard baseline levels without the genetic lowering effect seen in carriers of the minor allele [1]. This common genotype is highly prevalent across global populations, representing the standard genetic baseline for lipid clearance [2]. Lacking the protective T allele means there is a typical, standard risk for developing hypertriglyceridemia under high-carbohydrate diets [3]. Standard clinical lipid panels will reflect general lifestyle, diet, and overall polygenic influences rather than any specific protective benefit from this locus [4]. Uric acid or urate levels also tend to align with typical population averages [5]. Maintaining a balanced diet low in simple sugars remains highly effective for supporting healthy lipid profiles [6]. Overall cardiovascular risk from this specific marker is typical, meaning standard lifestyle factors play the primary role in lipid management [4]. Regular physical activity and monitoring of lipid levels are standard recommendations for maintaining metabolic health [7].
Typical fasting triglyceride levels; Typical HDL cholesterol levels; Standard baseline risk for hypertriglyceridemia.
Sample genotype: CT (Heterozygous)
Fasting triglyceride levels are significantly lower compared to the common genotype, providing a natural metabolic advantage [1]. This effect is driven by the presence of one copy of the protective T allele, which is linked to more efficient lipid processing [2]. Concurrently, levels of high-density lipoprotein, often called the good cholesterol, tend to be slightly elevated [3]. Such a dual effect of lower triglycerides and higher HDL is highly favorable for long-term cardiovascular health [4]. The risk of developing severe hypertriglyceridemia is also reduced, even when dietary carbohydrate intake is relatively high [5]. Serum urate levels may also be slightly lower, which is beneficial for joint and metabolic health [6]. These metabolic benefits are well-documented across diverse ancestral groups [7]. Adopting a heart-healthy lifestyle further enhances these inherent genetic advantages [8].
Lower fasting triglyceride levels; Slightly higher HDL cholesterol levels; Reduced risk of hypertriglyceridemia.
Sample genotype: TT (Homozygous)
Fasting triglyceride levels are at their lowest baseline due to carrying two copies of the protective T allele [1]. This genotype is relatively rare, occurring in only about one to two percent of most populations [2]. The metabolic clearance of fats is highly efficient, which significantly lowers the risk of lipid accumulation in the bloodstream [3]. High-density lipoprotein levels are typically at their highest, further supporting arterial and cardiovascular health [4]. Protection against severe hypertriglyceridemia is maximized with this genetic profile [5]. Additionally, circulating urate levels are lower, reducing the genetic predisposition to conditions related to high uric acid [6]. These combined lipid-lowering effects provide a robust buffer against common metabolic stressors [7]. Even with these favorable genetics, maintaining balanced nutrition supports overall metabolic longevity [8].
Lowest fasting triglyceride levels; Highest HDL cholesterol levels; Strong protection against hypertriglyceridemia.
Variants with shared genetic architecture
rs149793040 · ACACB Gene · Chr 12 · Triglyceride Levels
rs11429307 · C5orf67 Gene · Chr 5 · Triglyceride Levels
rs684773 · PCCB Gene · Chr 3 · Triglyceride Levels
Biological, clinical and population relevance of 95 loci for blood lipids.
Discovery and refinement of loci associated with lipid levels.
Effects of genetic variants on lipid parameters and dyslipidemia in a Chinese population.
Newly identified loci that influence lipid concentrations and risk of coronary artery disease.
Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels.
Content updated August 2026.
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