Abstract 15575: Polymorphism at the Telomerase Ribonucleic Acid Component Gene Interacts With Mediterranean Diet to Influence Inflammation Status and its Relationship With Telomere Attrition, From the CORDIOPREV Clinical Trial
Introduction: Telomere attrition has been associated with several age-related diseases such as cardiovascular disease. Telomerase RNA Component (TERC) genetic variants have been associated with leukocyte telomere length (LTL); whereas fatty acids are key metabolic regulators that can interact with genetic factors and influence in age-related diseases.
Hypothesis: To evaluate whether genetic variability at the TERC gene interacts with fatty acid profile and two healthy diets (low-fat diet, < 30% fat: 12-14% MUFA vs. Mediterranean diet enriched in olive oil, 35% fat: 22% MUFA) modulating LTL, inflammation status and glucose metabolism in patients with coronary heart disease (CHD).
Methods: Inflammation status (high sensitivity C-reactive protein (hsCRP)), glucose metabolism (glucose, insulin, glycated haemoglobin (HbA1c) and homeostasis model assessment of insulin resistance (HOMA-IR)), fatty acids, LTL and single nucleotide polymorphisms (SNPs) of the TERC gene (rs12696304, rs16847897 and rs3772190) were determined in 1,002 patients from the CORDIOPREV clinical trial (NCT00924937).
Results: We report an interaction between TERC rs12696304 SNP and plasma total MUFA levels affecting hsCRP (P =0.03) and LTL (P =0.01). Among subjects with MUFA levels above the median, carriers of the CC genotype showed lower hsCRP and higher LTL than G-allele carriers (GG + CG). After 12 months of dietary intervention, we found also a significant gene–diet interaction between TERC rs12696304 SNP and Mediterranean diet (P =0.03). Specifically, CC subjects displayed a greater decrease in hsCRP than G-allele carriers.
Conclusions: Our findings suggest that the TERC rs12696304 SNP interacts with MUFA improving inflammation status and telomere attrition related with CHD.
Moreover, Mediterranean diet intervention induced a better inflammatory profile in CC subjects compared with the G-allele carriers. Our results add further support to the concept of personalised nutritional advice tailored to the genetic make-up of CHD patients.
Author Disclosures: F. Gomez-Delgado: None. A. Garcia-Rios: None. I. Perez-Corral: None. A. Corina: None. J. Delgado-Lista: None. O. Rangel: None. J. Alcala-Diaz: None. J. Lopez-Miranda: None. P. Perez-Martinez: None.
- © 2016 by American Heart Association, Inc.