rs13236689 — CD36

Intronic CD36 variant that acts as a platelet eQTL, modulating CD36 surface expression and influencing platelet activation, oxidized-LDL uptake, and postprandial lipid handling.

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CD36 rs13236689 — Fat Sensing, Platelet Activation, and Cardiovascular Risk

CD36 (also called fatty acid translocase, or FAT) is one of the body's key gatekeepers for dietary fat. It sits on the surface of cells throughout the intestine, tongue taste buds, platelets, macrophages, muscle, and adipose tissue. Its job is to bind long-chain fatty acids — the molecules that make up most of the fat in food — and shuttle them into cells. When CD36 expression is higher, cells take up more fat; when it is lower, fat stays in the bloodstream longer. rs13236689 is an intronic variant11 intronic variant
A variant within a non-coding intron of the CD36 gene; these often act as expression regulators by altering transcription factor binding sites in the surrounding DNA that modulates how much CD36 protein cells produce.

The Mechanism

rs13236689 does not change the CD36 protein sequence — it lies within an intron on chromosome 7 at position 80,606,698 (GRCh38). Its biological significance lies in its status as a platelet expression quantitative trait locus (eQTL)22 platelet expression quantitative trait locus (eQTL)
An eQTL is a genomic variant that explains variation in how much of a gene's mRNA — and ultimately protein — is produced in a given tissue. Carriers of the G allele are in strong linkage disequilibrium with the functional regulatory variants rs2366739 and rs1194196, which sit approximately 13–55 kb upstream of the CD36 transcriptional start site and alter transcription factor binding. When these regulatory variants are active, platelet CD36 mRNA and surface protein levels increase. Higher platelet CD36 means stronger responses to oxidized LDL (oxLDL) — the chemically modified form of cholesterol that accumulates in atherosclerotic plaques — and greater platelet activation in lipid-rich environments.

The metabolic consequences extend beyond platelets. In the gut, enterocyte CD36 expression levels determine how efficiently long-chain fatty acids trigger satiety signals: CD36 converts dietary fatty acids into oleoylethanolamide (OEA)33 oleoylethanolamide (OEA)
A bioactive lipid that activates PPARα in the gut wall, sending a sustained satiety signal to the brain via the vagus nerve, which in turn activates PPARα to prolong the feeling of fullness after a fat-rich meal. Variants that push CD36 expression higher also increase uptake of oxLDL by macrophages in artery walls — a key step in foam cell formation and atherosclerosis.

The Evidence

The primary genetic evidence for rs13236689 comes from the COGENT consortium meta-analysis44 COGENT consortium meta-analysis
Cheng et al. (2012), PLoS Genetics — a meta-analysis of 7 genome-wide association studies in over 16,000 African Americans from population-based cohorts, which identified rs13236689 as a genome-wide significant locus for platelet count (p = 2.84×10⁻⁹; β = +4.18 × 10⁹ platelets/L per G allele). The association nominally replicated in European Americans. The same variant was subsequently shown by Madan et al. (2019, PLoS Genetics)55 Madan et al. (2019, PLoS Genetics)
Using a massively parallel reporter assay to screen 81 CD36 eQTLs, the authors confirmed that rs13236689 is a bona fide eQTL for platelet CD36 mRNA, with the causal signal mapping to two nearby regulatory variants (rs2366739, rs1194196) in high LD to be a platelet CD36 eQTL: G allele carriers have higher platelet CD36 surface expression.

The downstream cardiovascular significance of CD36 expression variation is well-established: higher platelet CD36 augments oxLDL-induced platelet activation and has been associated with thromboembolism risk. At the gene level, Love-Gregory et al. (2008)66 Love-Gregory et al. (2008)
Population study of 2,020 African Americans from the HyperGEN cohort; PMID 18305138 showed that multiple CD36 variants modulate HDL-C, triglycerides, and metabolic syndrome risk. The CD36 AGGIG haplotype in Caucasians was associated with 31% higher free fatty acids and OR 2.3 for cardiovascular events in type 2 diabetics (Corpeleijn et al. 2006, PMID 15282206)77 (Corpeleijn et al. 2006, PMID 15282206).

Evidence for rs13236689's direct effect on dietary fat handling and plasma lipids is moderate — the lipid associations are inferred from the eQTL relationship and the well-established biology of CD36 expression, rather than from dedicated dietary intervention trials targeting this specific variant.

Practical Actions

Because rs13236689 G allele carriers have higher platelet CD36 expression, they are likely to mount stronger platelet responses to circulating oxidized LDL. This is most relevant in the context of a diet high in saturated and trans fats, which drive oxLDL production. Limiting foods that generate oxLDL — principally processed and ultra-processed foods containing oxidized vegetable oils and trans fats — is directly relevant to this genotype. Longer-chain omega-3 fatty acids (EPA/DHA) compete with pro-inflammatory fatty acids at the CD36 binding site and have been shown to reduce platelet activation. Monitoring fasting triglycerides and HDL-C provides a practical window into CD36-mediated fat metabolism; the CD36 eQTL mechanism links directly to postprandial lipemia.

Interactions

rs13236689 is in linkage disequilibrium with other CD36 expression-regulating variants. The most studied CD36 SNP, rs1761667 (promoter, −31118G>A), directly affects fat taste sensitivity — AA homozygotes have 8-fold higher detection thresholds for oleic acid, meaning they perceive fat less intensely and tend to eat more of it. If a person carries both rs13236689 G (higher CD36 in platelets/ macrophages) and rs1761667 AA (lower fat taste sensitivity from reduced tongue CD36), the combined effect — increased cardiovascular risk from platelet hyperactivation alongside blunted dietary fat sensing — warrants attention. rs3211938 is a CD36 truncation variant (stop-gain) that dramatically reduces CD36 protein; this variant is functionally distinct from rs13236689 and largely confined to African-ancestry populations.

Nutrient Interactions

long-chain fatty acids altered_metabolism
omega-3 fatty acids increased_need

Genotype Interpretations

What each possible genotype means for this variant.

TT Baseline CD36 Expression Normal

Standard CD36 expression; typical platelet and fat-metabolism function

You carry two copies of the T allele at rs13236689, the reference allele at this intronic CD36 position. This is associated with baseline CD36 expression levels in platelets and other tissues. About 33% of people globally share this genotype, and it is somewhat more common in European and African populations (~57% T allele frequency) than in East Asian or South Asian populations.

Your platelet CD36 surface levels are expected to be in the typical range, meaning your platelets respond to oxidized LDL at average intensity. Postprandial fat handling and fat taste sensitivity at this locus are not specifically altered compared to the population average.

GT Elevated CD36 Expression Intermediate

One G allele — moderately elevated platelet CD36 expression

Platelet CD36 acts as a receptor for oxidized phospholipids and oxLDL. When CD36 expression is elevated, platelets generate stronger activation signals in lipid-rich environments — an effect that matters most when circulating oxLDL is high (typically in people eating diets rich in processed, oxidized fats or with established dyslipidemia).

In the gut, enterocyte CD36 expression influences how strongly each fatty acid meal triggers satiety signaling via the OEA–PPARα axis. Moderately elevated CD36 from one G allele may enhance postprandial satiety slightly, but the primary documented phenotype at this locus is platelet-related.

GG High CD36 Expression High

Two G alleles — highest platelet CD36 expression at this locus

Platelet CD36 at elevated levels creates a heightened response to oxidized LDL and oxidized phospholipids found in atherosclerotic plaques and in the bloodstream of people eating high-oxidized-fat diets. Studies show that higher platelet CD36 expression correlates with stronger oxLDL-induced platelet activation and has been associated with thromboembolic risk.

The same G allele haplotype that increases platelet CD36 also upregulates CD36 in macrophages, promoting foam cell formation — the cellular hallmark of early atherosclerosis. In the gut, higher enterocyte CD36 facilitates more efficient long-chain fatty acid uptake; when dietary fat quality is poor (high in saturated and oxidized fats), this becomes a liability rather than an advantage, increasing chylomicron production and postprandial lipemia.

CD36 also mediates uptake of thrombospondin-1 (TSP-1) and beta-amyloid — broad ligand binding that becomes pro-inflammatory when CD36 expression is constitutively elevated. For the GG genotype, managing the quality and quantity of circulating oxLDL is the primary modifiable risk factor.