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Dietary linoleic acid interacts with FADS1 genetic variability to modulate HDL-cholesterol and obesity-related traits.
Clin Nutr. 2018 10; 37(5):1683-1689.CN

Abstract

BACKGROUND & AIMS

Blood levels of polyunsaturated fatty acids (PUFAs) are under control of endogenous synthesis via Δ5- and Δ6-desaturases, encoded by the FADS1 and FADS2 genes, respectively and of diet. Genome-wide associations studies (GWAS) reported associations between polymorphisms in FADS1-FADS2 and variations in plasma concentrations of PUFAs, HDL- and LDL-cholesterol and triglycerides. However, it is not established whether dietary PUFAs intake modulates these associations. We assessed whether dietary linoleic acid (LA) or α-linolenic acid (ALA) modulate the association between the FADS1 rs174547 polymorphism (a GWAS hit) and lipid and anthropometric phenotypes.

METHODS

Dietary intakes of LA and ALA, FADS1 rs174547 genotypes, lipid and anthropometric variables were determined in three French population-based samples (n = 3069). These samples were stratified according to the median dietary LA (<9.5 and ≥9.5 g/d) and ALA (<0.80 and ≥0.80 g/d) intakes. The meta-analysis was performed using a random-effect.

RESULTS

Our meta-analysis confirmed the association between rs174547 and plasma lipid levels and revealed an association with waist circumference and body mass index. These associations were not modified by dietary ALA intake (all p-interaction > 0.05). In contrast, the associations with HDL-cholesterol levels, waist circumference and BMI were modulated by the dietary intake of LA (p interaction < 0.05). In high LA consumers only, the rs174547 minor allele was significantly associated with lower HDL-cholesterol levels (β = -0.05 mmol/L, p = 0.0002). Furthermore, each copy of the rs174547 minor allele was associated with a 1.58 cm lower waist circumference (p = 0.0005) and a 0.46 kg m-2 lower BMI (p = 0.01) in the low LA intake group, but not in the high LA intake group.

CONCLUSIONS

The present study suggests that dietary LA intake may modulate the association between the FADS gene variants and HDL-cholesterol concentration, waist circumference and BMI. These gene-nutrient interactions, if confirmed, suggest that subjects carrying the rs174547 minor allele might benefit from low dietary LA intakes.

Authors+Show Affiliations

Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France. Electronic address: julie.dumont-2@univ-lille2.fr.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.Laboratoire d'Épidémiologie et de Santé Publique, Fédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, EA 3430, F-67200 Strasbourg, France.Laboratoire d'Épidémiologie et de Santé Publique, Fédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, EA 3430, F-67200 Strasbourg, France.CarMen, INSERM 1060, University Lyon 1, INRA U1235, CRNH Rhônes-Alpes, F-69600 Lyon, France.UMR INSERM 1027, Département d'Épidémiologie et de Santé Publique, Université Paul Sabatier, Toulouse Purpan, F-31062 Toulouse, France.UMR INSERM 1027, Département d'Épidémiologie et de Santé Publique, Université Paul Sabatier, Toulouse Purpan, F-31062 Toulouse, France.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.Univ. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167, RID-AGE, Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, F-59000 Lille, France.

Pub Type(s)

Journal Article
Meta-Analysis
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28774683

Citation

Dumont, Julie, et al. "Dietary Linoleic Acid Interacts With FADS1 Genetic Variability to Modulate HDL-cholesterol and Obesity-related Traits." Clinical Nutrition (Edinburgh, Scotland), vol. 37, no. 5, 2018, pp. 1683-1689.
Dumont J, Goumidi L, Grenier-Boley B, et al. Dietary linoleic acid interacts with FADS1 genetic variability to modulate HDL-cholesterol and obesity-related traits. Clin Nutr. 2018;37(5):1683-1689.
Dumont, J., Goumidi, L., Grenier-Boley, B., Cottel, D., Marécaux, N., Montaye, M., Wagner, A., Arveiler, D., Simon, C., Ferrières, J., Ruidavets, J. B., Amouyel, P., Dallongeville, J., & Meirhaeghe, A. (2018). Dietary linoleic acid interacts with FADS1 genetic variability to modulate HDL-cholesterol and obesity-related traits. Clinical Nutrition (Edinburgh, Scotland), 37(5), 1683-1689. https://doi.org/10.1016/j.clnu.2017.07.012
Dumont J, et al. Dietary Linoleic Acid Interacts With FADS1 Genetic Variability to Modulate HDL-cholesterol and Obesity-related Traits. Clin Nutr. 2018;37(5):1683-1689. PubMed PMID: 28774683.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary linoleic acid interacts with FADS1 genetic variability to modulate HDL-cholesterol and obesity-related traits. AU - Dumont,Julie, AU - Goumidi,Louisa, AU - Grenier-Boley,Benjamin, AU - Cottel,Dominique, AU - Marécaux,Nadine, AU - Montaye,Michèle, AU - Wagner,Aline, AU - Arveiler,Dominique, AU - Simon,Chantal, AU - Ferrières,Jean, AU - Ruidavets,Jean-Bernard, AU - Amouyel,Philippe, AU - Dallongeville,Jean, AU - Meirhaeghe,Aline, Y1 - 2017/07/20/ PY - 2017/01/18/received PY - 2017/07/13/revised PY - 2017/07/13/accepted PY - 2017/8/5/pubmed PY - 2019/11/19/medline PY - 2017/8/5/entrez KW - Diet KW - FADS1 gene KW - Fatty acid KW - Linoleic acid KW - Lipid KW - Obesity SP - 1683 EP - 1689 JF - Clinical nutrition (Edinburgh, Scotland) JO - Clin Nutr VL - 37 IS - 5 N2 - BACKGROUND & AIMS: Blood levels of polyunsaturated fatty acids (PUFAs) are under control of endogenous synthesis via Δ5- and Δ6-desaturases, encoded by the FADS1 and FADS2 genes, respectively and of diet. Genome-wide associations studies (GWAS) reported associations between polymorphisms in FADS1-FADS2 and variations in plasma concentrations of PUFAs, HDL- and LDL-cholesterol and triglycerides. However, it is not established whether dietary PUFAs intake modulates these associations. We assessed whether dietary linoleic acid (LA) or α-linolenic acid (ALA) modulate the association between the FADS1 rs174547 polymorphism (a GWAS hit) and lipid and anthropometric phenotypes. METHODS: Dietary intakes of LA and ALA, FADS1 rs174547 genotypes, lipid and anthropometric variables were determined in three French population-based samples (n = 3069). These samples were stratified according to the median dietary LA (<9.5 and ≥9.5 g/d) and ALA (<0.80 and ≥0.80 g/d) intakes. The meta-analysis was performed using a random-effect. RESULTS: Our meta-analysis confirmed the association between rs174547 and plasma lipid levels and revealed an association with waist circumference and body mass index. These associations were not modified by dietary ALA intake (all p-interaction > 0.05). In contrast, the associations with HDL-cholesterol levels, waist circumference and BMI were modulated by the dietary intake of LA (p interaction < 0.05). In high LA consumers only, the rs174547 minor allele was significantly associated with lower HDL-cholesterol levels (β = -0.05 mmol/L, p = 0.0002). Furthermore, each copy of the rs174547 minor allele was associated with a 1.58 cm lower waist circumference (p = 0.0005) and a 0.46 kg m-2 lower BMI (p = 0.01) in the low LA intake group, but not in the high LA intake group. CONCLUSIONS: The present study suggests that dietary LA intake may modulate the association between the FADS gene variants and HDL-cholesterol concentration, waist circumference and BMI. These gene-nutrient interactions, if confirmed, suggest that subjects carrying the rs174547 minor allele might benefit from low dietary LA intakes. SN - 1532-1983 UR - https://www.unboundmedicine.com/medline/citation/28774683/Dietary_linoleic_acid_interacts_with_FADS1_genetic_variability_to_modulate_HDL_cholesterol_and_obesity_related_traits_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0261-5614(17)30253-4 DB - PRIME DP - Unbound Medicine ER -