rs3211883 — CD36

Intronic CD36 variant associated with altered body adiposity and platelet CD36 expression; the minor A allele tags a haplotype linked to higher waist circumference and BMI, reflecting CD36's role in long-chain fatty acid sensing and uptake

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CD36 — Fat Sensor, Scavenger Receptor, and Metabolic Gatekeeper

CD3611 CD36
CD36 molecule (also known as fatty acid translocase, FAT, or glycoprotein IV); a multifunctional class B scavenger receptor expressed on platelets, macrophages, adipocytes, enterocytes, skeletal muscle, and taste receptor cells performs a striking number of jobs simultaneously: it transports long-chain fatty acids across cell membranes, senses dietary fat on the tongue and in the gut, mediates uptake of oxidized LDL into macrophages (a key step in atherosclerotic plaque formation), and coordinates chylomicron assembly in intestinal epithelial cells. The rs3211883 variant sits deep in an intron of the CD36 gene on chromosome 7 and, while it does not directly change the protein sequence, it tags a haplotype that appears to modulate CD36 expression levels — with downstream consequences for fat handling and body composition.

The Mechanism

As an intronic variant22 intronic variant
A DNA change located within a non-coding intron; intronic variants typically act by altering regulatory elements, splice enhancers, or gene expression rather than changing the amino acid sequence of the protein, rs3211883 does not directly alter the CD36 protein. Instead, it marks a haplotype block that correlates with differences in CD36 surface expression on platelets — a finding documented in genome-wide association studies of CD36 expression quantitative trait loci. Lower CD36 expression in intestinal enterocytes reduces the protein's ability to coordinate chylomicron33 chylomicron
Chylomicrons are large lipid-transporting particles assembled in intestinal cells after a fatty meal; they shuttle dietary fat from the gut into the lymphatic system and then into the bloodstream assembly from dietary fatty acids, potentially altering the rate at which long-chain fats move from the gut into circulation. Altered CD36 expression also affects fat taste perception — individuals with lower CD36 expression show reduced oral sensitivity to oleic acid, which may blunt the satiety signals normally triggered by fat consumption and contribute to higher overall energy intake.

The Evidence

The most direct evidence for rs3211883 comes from a study of 646 European adolescents by Bokor et al. (2010)44 Bokor et al. (2010)
Bokor S et al. Single-nucleotide polymorphism of CD36 locus and obesity in European adolescents. Obesity (Silver Spring), 2010, which found that carriers of the minor A allele had a significantly elevated odds ratio for obesity of 1.73 (95% CI 1.16–2.59, P=0.007). The association extended to higher BMI and body fat percentage in the validation cohort. A haplotype carrying the minor alleles of four CD36 SNPs — including rs3211883 — was associated with even higher obesity risk (OR 2.28, P=0.0008).

However, a subsequent meta-analysis by Choquet et al. (2011)55 meta-analysis by Choquet et al. (2011)
Choquet H et al. Lack of association of CD36 SNPs with early onset obesity: a meta-analysis in 9,973 European subjects. Obesity (Silver Spring), 2011 combining data from 9,973 European subjects found no significant association of rs3211883 with obesity risk (P=0.66). This discrepancy is common in early-generation genetic association studies and reflects the modest effect size of individual intronic variants whose primary role is haplotype-tagging rather than direct functional change.

Stronger evidence emerged from Heni et al. (2011)66 Heni et al. (2011)
Heni M et al. Variants in the CD36 gene locus determine whole-body adiposity, but have no independent effect on insulin sensitivity. Obesity, 2011, who genotyped six CD36 SNPs tagging all common variation in the gene in 1,790 Europeans at risk for type 2 diabetes. rs3211883 and rs3211908 were among the variants that significantly associated with waist circumference after Bonferroni correction (P<0.0042). Critically, no independent effect on insulin sensitivity was detected — suggesting the variant affects metabolic risk primarily through its influence on fat distribution rather than direct insulin signaling.

On the molecular side, genome-wide association studies of platelet CD36 surface expression have linked rs3211883 to measured CD36 protein levels (P=0.000298, β=0.69), providing a plausible intermediate mechanism: the variant's haplotype influences how much CD36 protein is produced, which then affects both platelet activation responses to oxidized LDL and intestinal fat handling.

A population-specific finding came from a Japanese cohort study77 Japanese cohort study
Kondo N et al. Positive association of common variants in CD36 with neovascular age-related macular degeneration. Aging (Albany NY), 2009 of 109 neovascular AMD cases and 182 controls, where the A allele was actually protective against AMD (OR 0.50, P=2.09×10⁻⁴ after Bonferroni correction). This underscores that the allele's effects are context- and tissue-specific: the same variant that tags increased adiposity risk in Western European populations may have neutral or even protective effects in retinal vasculature in East Asian populations.

Practical Actions

The A allele's primary documented effect is on body fat distribution — specifically waist circumference and overall adiposity. Since CD36 regulates the gut's fat-sensing machinery, individuals with the A allele may benefit from dietary strategies that compensate for altered fat absorption signaling. The protein's established role in long-chain saturated fatty acid transport means that dietary fat composition — not just quantity — is relevant. High saturated fat loads may overwhelm altered CD36 signaling in ways that unsaturated fats do not.

Given the A allele's association with higher platelet CD36 expression in some studies and CD36's role in oxidized LDL uptake by macrophages, monitoring of cardiovascular lipid markers is reasonable for A allele carriers, particularly if other cardiovascular risk factors are present.

Interactions

rs3211883 is in partial linkage disequilibrium with other functional CD36 variants, most notably rs1761667 (associated with oral fat perception and CD36 expression) and rs1527483 (linked to fat taste preferences and triglyceride levels). Individuals carrying the A allele at rs3211883 alongside the A allele at rs1761667 may have compounding impairments in dietary fat sensing that amplify the risk of excess energy intake from high-fat foods. The rs3173798 variant, which sits nearby in the CD36 gene and showed association with AMD in the same Japanese cohort, is in strong LD with rs3211883 in East Asian populations — indicating these two SNPs likely tag the same underlying haplotype in that ancestry group.

Nutrient Interactions

long-chain fatty acids altered_metabolism
dietary fat altered_metabolism

Genotype Interpretations

What each possible genotype means for this variant.

TT Standard Fat Metabolism Normal

Common CD36 variant pattern — standard fat sensing and adiposity profile

You carry two copies of the T allele at rs3211883, the major allele in most populations (approximately 90% frequency in Europeans). This genotype corresponds to the population-typical CD36 haplotype associated with normal intestinal fatty acid sensing and average adiposity measures in association studies. The Heni et al. (2011) study of 1,790 Europeans found no significant association between TT homozygosity and elevated waist circumference or BMI after Bonferroni correction. About 81% of Europeans carry the TT or AT genotype; this result covers TT homozygotes specifically.

AT Carrier — Mildly Elevated Risk Intermediate

One copy of the A allele — modestly elevated waist circumference association

You carry one copy of the minor A allele at rs3211883. The Heni et al. (2011) study found that the A allele associates with higher waist circumference in an additive pattern, meaning one copy confers an intermediate effect between the TT and AA genotypes. The absolute effect size is modest — this is a common intronic variant tagging a haplotype rather than a direct functional change. Approximately 17% of Europeans carry the AT genotype (reflecting the ~10% A allele frequency in European populations). In African populations where the A allele reaches ~55%, nearly half of individuals carry the AT genotype. The Bokor 2010 study found that carrying the minor allele increased obesity odds by 1.73-fold in adolescents, though larger meta-analyses have not replicated the obesity association with statistical significance.

AA Homozygous Minor Allele High Risk

Two copies of the A allele — highest genotype-based adiposity association

You carry two copies of the minor A allele at rs3211883, the rarest genotype at this locus — approximately 1% frequency in Europeans (using Hardy-Weinberg from 10% allele frequency). This genotype sits at the top of the additive risk gradient documented for this variant. The Heni et al. (2011) study found that variants at this CD36 locus (including rs3211883) significantly associated with waist circumference and BMI after stringent Bonferroni correction for multiple testing. The A allele is more common in African (55%) and East Asian (38%) populations, so AA homozygosity, while rare in Europeans, is relatively more common in individuals with African ancestry. The Bokor 2010 adolescent study reported an OR of 1.73 per minor allele for obesity, projecting to approximately 3-fold higher odds for AA homozygotes if the effect is truly additive.