Abstract
Our group built a genetic risk score (GRS) of the plasma triglyceride (TG) response to an omega-3 (n-3) fatty acid (FA) supplementation in Caucasian Canadians that explained 21.53% of the TG variance. The objective was to refine the GRS by fine mapping and to test its association with the TG response in young Mexican adults. A total of 191 participants underwent a 6-week n-3 FA supplementation providing 2.7g/day of docosahexaenoic and eicosapentaenoic acids. Using quantitative polymerase chain reaction (PCR), 103 single-nucleotide polymorphisms (SNPs) were genotyped. A stepwise regression adjusted for age, sex, and body mass index (BMI) was used to select the strongest SNPs to include in the genetic risk model. A GRS was calculated from the sum of at-risk alleles. The contribution of the GRS to the TG response was assessed by ANCOVA with age, sex, and BMI included in the model. Several differences in allele frequency were observed between Canadians and Mexicans. Five lead SNPs were included in the genetic risk model, in which the GRS accounted for 11.01% of the variance of the TG response (p < 0.0001). These findings highlight the important contribution of genetic factors to the heterogeneity of the TG response to an n-3 FA supplementation among Mexicans.
Highlights
The metabolic response to a treatment or a dietary intervention, even when proven effective, can vary considerably from one individual to another, sometimes resulting in an even more deteriorated profile after the treatment or the intervention [1,2,3,4,5]
A proportion of 40.8% of the Mexican population was non-responsive to the n-3 fatty acid (FA) supplementation, as opposed to 59.2% of responders
Our findings show that the genetic risk score (GRS) accounts for a larger proportion of the TG variance when participants with the lowest magnitude of TG response are excluded from the calculation
Summary
The metabolic response to a treatment or a dietary intervention, even when proven effective, can vary considerably from one individual to another, sometimes resulting in an even more deteriorated profile after the treatment or the intervention [1,2,3,4,5]. In this sense, numerous studies have demonstrated that the metabolic response to an omega-3 (n-3) fatty acid (FA) supplementation, at pharmacological doses, is highly heterogeneous, and so is the plasma triglyceride (TG) response [6,7]. Results have been replicated in participants of the European FINGEN Study [15]
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