Interaction of genetics risk score (GRS) and fatty acids quality indices on healthy and unhealthy obesity phenotype

Author:

Rasaei Niloufar1,Fatemi Seyedeh Fatemeh2,Gholami Fatemeh1,Samadi Mahsa1,Mohammadian Mohammad Keshavarz3,Mirzaei Khadijeh1

Affiliation:

1. Tehran University of Medical Sciences (TUMS)

2. Mashhad University of Medical Sciences

3. Islamic Azad University

Abstract

Abstract Background: The growth in obesity and rates of abdominal obesity in developing countries is due to the dietary transition. Environmental changes, such as increasing the quality of dietary fat consumed, may be useful in prevent or improvement the obesity or unhealthy obesity phenotype in persons who are genetically predisposed to it, although this is not yet firmly established. Therefore, in the current study, we look at how dietary fat quality indices with metabolically healthy obesity (MHO) or metabolically unhealthy obesity (MUO) based on Karelis criteria interact with genetic predisposition in Iranian female adults. Methods: 279 obese and overweight women participated in the current cross-sectional investigation. Dietary assessment was done using a 147-item food frequency questionnaire (FFQ) and dietary fat quality was assessed by cholesterol-saturated fat index (CSI) and the ratio of omega-6/omega-3 (N6/N3) essential fatty acids. Three single nucleotide polymorphisms—MC4R (rs17782313), CAV-1 (rs3807992), and Cry-1(rs2287161) were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique and were combined to produce the genetic risk score (GRS). Using a multi-frequency bioelectrical impedance analyzer, body composition was evaluated. The participants were divided into MHO or MUO phenotypes after the metabolic risk was evaluated using Karelis criteria. Results: We found significant interactions between GRS and N6/N3 in adjusted model controlling for confounding factors (age, BMI, energy, and physical activity) (β= 2.26, 95% CI= 0.008–4.52, P= 0.049). In addition, we discovered marginal significant interactions between GRS and N6/N3 in crude (β= 1.92, 95% CI= -0.06–3.91, P= 0.058) and adjusted (age and energy) (β= 2.00, 95% CI= -0.05–4.05, P= 0.057) models on MUH obesity phenotype. However, no significant interactions between GRS and CSI were shown in both crude and adjusted models. Conclusion: This study highlights the importance of personalized nutrition and recommends further study of widely varying fat intake based on the findings on gene-N6/N3 PUFA interactions.

Publisher

Research Square Platform LLC

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