PD559 - ASSOCIATION OF CLOCK RS1801260 POLYMORPHISM WITH ADIPOSITY AND CARDIOMETABOLIC MARKERS

PD559

ASSOCIATION OF CLOCK RS1801260 POLYMORPHISM WITH ADIPOSITY AND CARDIOMETABOLIC MARKERS

H. G. Ulusoy Gezer^1,*, A. O. İşler², S. H. Oğuz², E. Karabulut³, N. Rakıcıoğlu¹

¹Department of Nutrition and Dietetics, Faculty of Health Sciences, ²Division of Endocrinology and Metabolism, Department of Internal Medicine, ³Department of Biostatistics, School of Medicine, Hacettepe University, Ankara, Türkiye

Rationale: The circadian gene CLOCK has been implicated in obesity susceptibility, insulin resistance, and lipid metabolism. However, findings on the rs1801260 polymorphism remain inconsistent across populations, and evidence on gene-diet interactions is limited. This study examined the association between the CLOCK rs1801260 polymorphism and adiposity, insulin resistance, and atherogenic index of plasma (AIP) and evaluated potential interaction with Mediterranean diet adherence.

Methods: A total of 443 adults (healthy bodyweight: n=211; overweight/obesity: n=232) were included. Genotypes were analyzed using codominant, additive, and dominant models. Minor allele frequency (MAF) and Hardy-Weinberg equilibrium (HWE) were assessed. Insulin resistance was estimated using log-transformed HOMA-IR, and cardiometabolic risk was assessed using AIP. Multivariable linear regression models were adjusted for age and sex. Gene-diet interaction was tested using centered variables and hierarchical regression.

Results: Genotype distribution did not differ between bodyweight groups (p=0.517). HWE was satisfied in all samples (p>0.80), and overall MAF was 0.30. In regression analyses, rs1801260 genotype was not associated with body fat percentage (p=0.332), log(HOMA-IR) (p=0.690), or AIP (p=0.229). The interaction between CLOCK genotype and Mediterranean diet adherence did not improve model fit for adiposity (ΔR²=0.001; p=0.391) or AIP (ΔR²<0.001; p=0.994).

Conclusion: In this study, CLOCK rs1801260 polymorphism was not independently associated with adiposity, insulin resistance, or atherogenic risk, nor was there evidence of gene-diet interaction. These findings suggest that the metabolic impact of this variant may be modest or population-specific.

Disclosure of Interest: H. Ulusoy Gezer Grant / Research Support from: This study was supported by the Health Institutes of Türkiye (TÜSEB) (Project Number: 43490)., A. İşler: None declared, S. Oğuz: None declared, E. Karabulut: None declared, N. Rakıcıoğlu: None declared