Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases

Nutrients

Floyd H. Chilton¹  Robert C. Murphy²  Bryan A. Wilson³  Susan Sergeant¹  Hannah Ainsworth³  Michael C. Seeds¹ 

[1] The Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA; E-Mails:;Department of Pharmacology, University of Colorado Denver, Aurora, CO 80045, USA; E-Mail:;Molecular Medicine and Translational Sciences, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA; E-Mails:

关键词: polyunsaturated fatty acids;    nutrition;    genetic variants;    fatty acid desaturase (FADS);    single nucleotide polymorphisms;    arachidonic acid;    eicosanoids;    inflammation;    cardiovascular disease;   

DOI  :  10.3390/nu6051993

来源: mdpi

【 摘 要 】

The “modern western” diet (MWD) has increased the onset and progression of chronic human diseases as qualitatively and quantitatively maladaptive dietary components give rise to obesity and destructive gene-diet interactions. There has been a three-fold increase in dietary levels of the omega-6 (n-6) 18 carbon (C18), polyunsaturated fatty acid (PUFA) linoleic acid (LA; 18:2n-6), with the addition of cooking oils and processed foods to the MWD. Intense debate has emerged regarding the impact of this increase on human health. Recent studies have uncovered population-related genetic variation in the LCPUFA biosynthetic pathway (especially within the fatty acid desaturase gene (FADS) cluster) that is associated with levels of circulating and tissue PUFAs and several biomarkers and clinical endpoints of cardiovascular disease (CVD). Importantly, populations of African descent have higher frequencies of variants associated with elevated levels of arachidonic acid (ARA), CVD biomarkers and disease endpoints. Additionally, nutrigenomic interactions between dietary n-6 PUFAs and variants in genes that encode for enzymes that mobilize and metabolize ARA to eicosanoids have been identified. These observations raise important questions of whether gene-PUFA interactions are differentially driving the risk of cardiovascular and other diseases in diverse populations, and contributing to health disparities, especially in African American populations.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.