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Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids

OBJECTIVE: SNPs identified from genome-wide association studies associate with lipid risk markers of cardiovascular disease. This study investigated whether these SNPs altered the plasma lipid response to diet in the ‘RISCK’ study cohort. METHODS: Participants (n = 490) from a dietary intervention t...

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Autores principales: Walker, C.G., Loos, R.J.F., Olson, A.D., Frost, G.S., Griffin, B.A., Lovegrove, J.A., Sanders, T.A.B., Jebb, S.A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407860/
https://www.ncbi.nlm.nih.gov/pubmed/21292264
http://dx.doi.org/10.1016/j.atherosclerosis.2010.12.039
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author Walker, C.G.
Loos, R.J.F.
Olson, A.D.
Frost, G.S.
Griffin, B.A.
Lovegrove, J.A.
Sanders, T.A.B.
Jebb, S.A.
author_facet Walker, C.G.
Loos, R.J.F.
Olson, A.D.
Frost, G.S.
Griffin, B.A.
Lovegrove, J.A.
Sanders, T.A.B.
Jebb, S.A.
author_sort Walker, C.G.
collection PubMed
description OBJECTIVE: SNPs identified from genome-wide association studies associate with lipid risk markers of cardiovascular disease. This study investigated whether these SNPs altered the plasma lipid response to diet in the ‘RISCK’ study cohort. METHODS: Participants (n = 490) from a dietary intervention to lower saturated fat by replacement with carbohydrate or monounsaturated fat, were genotyped for 39 lipid-associated SNPs. The association of each individual SNP, and of the SNPs combined (using genetic predisposition scores), with plasma lipid concentrations was assessed at baseline, and on change in response to 24 weeks on diets. RESULTS: The associations between SNPs and lipid concentrations were directionally consistent with previous findings. The genetic predisposition scores were associated with higher baseline concentrations of plasma total (P = 0.02) and LDL (P = 0.002) cholesterol, triglycerides (P = 0.001) and apolipoprotein B (P = 0.004), and with lower baseline concentrations of HDL cholesterol (P < 0.001) and apolipoprotein A-I (P < 0.001). None of the SNPs showed significant association with the reduction of plasma lipids in response to the dietary interventions and there was no evidence of diet-gene interactions. CONCLUSION: Results from this exploratory study have shown that increased genetic predisposition was associated with an unfavourable plasma lipid profile at baseline, but did not influence the improvement in lipid profiles by the low-saturated-fat diets.
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spelling pubmed-34078602012-08-06 Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids Walker, C.G. Loos, R.J.F. Olson, A.D. Frost, G.S. Griffin, B.A. Lovegrove, J.A. Sanders, T.A.B. Jebb, S.A. Atherosclerosis Article OBJECTIVE: SNPs identified from genome-wide association studies associate with lipid risk markers of cardiovascular disease. This study investigated whether these SNPs altered the plasma lipid response to diet in the ‘RISCK’ study cohort. METHODS: Participants (n = 490) from a dietary intervention to lower saturated fat by replacement with carbohydrate or monounsaturated fat, were genotyped for 39 lipid-associated SNPs. The association of each individual SNP, and of the SNPs combined (using genetic predisposition scores), with plasma lipid concentrations was assessed at baseline, and on change in response to 24 weeks on diets. RESULTS: The associations between SNPs and lipid concentrations were directionally consistent with previous findings. The genetic predisposition scores were associated with higher baseline concentrations of plasma total (P = 0.02) and LDL (P = 0.002) cholesterol, triglycerides (P = 0.001) and apolipoprotein B (P = 0.004), and with lower baseline concentrations of HDL cholesterol (P < 0.001) and apolipoprotein A-I (P < 0.001). None of the SNPs showed significant association with the reduction of plasma lipids in response to the dietary interventions and there was no evidence of diet-gene interactions. CONCLUSION: Results from this exploratory study have shown that increased genetic predisposition was associated with an unfavourable plasma lipid profile at baseline, but did not influence the improvement in lipid profiles by the low-saturated-fat diets. Elsevier 2011-04 /pmc/articles/PMC3407860/ /pubmed/21292264 http://dx.doi.org/10.1016/j.atherosclerosis.2010.12.039 Text en © 2011 Elsevier Ireland Ltd. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license
spellingShingle Article
Walker, C.G.
Loos, R.J.F.
Olson, A.D.
Frost, G.S.
Griffin, B.A.
Lovegrove, J.A.
Sanders, T.A.B.
Jebb, S.A.
Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids
title Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids
title_full Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids
title_fullStr Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids
title_full_unstemmed Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids
title_short Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids
title_sort genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407860/
https://www.ncbi.nlm.nih.gov/pubmed/21292264
http://dx.doi.org/10.1016/j.atherosclerosis.2010.12.039
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