PD601 - ASSOCIATION OF CD36 RS1761667 POLYMORPHISM WITH DIETARY HABITS AND METABOLIC SYNDROME MARKERS

PD601

ASSOCIATION OF CD36 RS1761667 POLYMORPHISM WITH DIETARY HABITS AND METABOLIC SYNDROME MARKERS

N. Kenda^1,*, Z. Jenko Pražnikar¹, K. Kramberger¹

¹Faculty of Health Sciences, University of Primorska, Koper, Slovenia

Rationale: Interindividual variability in metabolic responses to diet reflects biological heterogeneity, including genetic differences in fat perception and lipid metabolism. The CD36 rs1761667 polymorphism has been linked to altered fat sensing; however, its association with habitual dietary intake and metabolic syndrome (MS) markers remains insufficiently defined.

Methods: This cross-sectional study included 141 healthy adults. CD36 rs1761667 genotypes were determined using polymerase chain reaction (PCR)-based methods. Dietary intake was assessed using validated questionnaires and food records. Anthropometric measures, including body mass index (BMI) and waist circumference, as well as blood markers of MS, including the lipid profile, fasting glucose, and C-reactive protein (CRP), were analysed according to CD36 genotype.

Results: A statistically significant difference in BMI was observed across CD36 rs1761667 genotype groups, with GG homozygotes exhibiting higher values than carriers of the A allele. Differences in waist circumference and blood markers did not reach statistical significance; however, the results consistently indicated a less favourable profile among GG homozygotes, particularly with respect to triglyceride concentrations and CRP levels. In contrast, AA homozygotes had lower triglyceride levels and a more favourable inflammatory profile, despite reporting less favourable dietary habits characterised by a higher intake of saturated fatty acids and simple carbohydrates.

Conclusion: The CD36 rs1761667 polymorphism is associated with differences in anthropometric measures and MS markers in healthy adults. The discordance between dietary patterns and metabolic profile suggests that genetic susceptibility may modulate metabolic risk independently of diet. These findings may inform future approaches to nutritional assessment and strategies for the prevention of MS.

Disclosure of Interest: None declared