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Interaction between lipoprotein lipase and apolipoprotein E gene polymorphisms and dietary factors on lipid traits

Published online by Cambridge University Press:  11 December 2017

I. Shatwan ,
B. Ellahi ,
K.H. Winther ,
Y. Ben-Shlomo ,
P.C. Elwood ,
I. Givens ,
M. Rayman ,
J.A. Lovegrove  and
K.S. Vimaleswaran
I. Shatwan
Affiliation:
Hugh Sinclair Unit of Human Nutrition, University of Reading, Whiteknights, Reading, UK, RG6 6AP, UK Food and Nutrition Department, Faculty of Home Economics, King Abdulaziz University, Jeddah, Saudi Arabia
B. Ellahi
Affiliation:
Faculty of Health and Social Care, University of Chester, Chester, CH1 1SL, UK
K.H. Winther
Affiliation:
EFE – Endocrine Elite Research Centre Department of Endocrinology and Metabolism Odense University Hospital Denmark
Y. Ben-Shlomo
Affiliation:
Department of Social Medicine, University of Bristol, Bristol, BS8 1TH, UK
P.C. Elwood
Affiliation:
Department of Epidemiology, Statistics and Public Health, Cardiff University, University Hospital of Wales, Heath Park, Cardiff, CF14 4XW, UK
I. Givens
Affiliation:
Centre for Food, Nutrition and Health, University of Reading, Arley Gate, Reading RG6 6AR, UK
M. Rayman
Affiliation:
Department of Nutritional Sciences Faculty of Health and Medical Sciences, University of Surrey Guildford, GU2 7XH, UK
J.A. Lovegrove
Affiliation:
Hugh Sinclair Unit of Human Nutrition, University of Reading, Whiteknights, Reading, UK, RG6 6AP, UK
K.S. Vimaleswaran
Affiliation:
Hugh Sinclair Unit of Human Nutrition, University of Reading, Whiteknights, Reading, UK, RG6 6AP, UK
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Abstract

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Altered serum lipid level is one of the risk factors for development of cardiovascular disease (CVD)( Reference Musunuru 1 ). Genetic association studies have identified loci in lipid metabolism-related genes such as lipoprotein lipase (LPL) and apolipoprotein E (APOE), which have been shown to be associated with lipid traits( Reference Shatwan 2 , Reference Bennet 3 ). However, very few studies have offered insight into how diet modifies the effect of LPL and APOE single nucleotide polymorphisms (SNPs) on lipids( Reference Carvalho-Wells 4 , Reference Nettleton 5 ). Hence, we investigated the association of common LPL (rs320 and rs328) and APOE SNPs (rs405509, rs439401, rs445925, rs405697, rs1160985, rs1064725, rs7412 and rs429358) with lipids and examined the interactions between the SNPs and dietary factors on lipids in two Caucasian populations. The populations include 664 individuals from the Prevention of Cancer by Intervention with Selenium (PRECISE) and 1,238 individuals from the Caerphilly study. Statistically significant association was detected between APOE haplotypes (rs7412 and rs429358) and APOE SNP rs445925 and total cholesterol (P = 0·0004 and P = 0·003, respectively). The carriers of APOE E2 allele (5·54± 0·97 mmol/L) had lowest total cholesterol levels compared with E3 allele (5·98± 1·05 mmol/L) (P = 0·001) and E4 allele (6·09± 1·06 mmol/L) (P = 0·0002) carriers, respectively. The association between APOE haplotypes and rs445925 and total cholesterol (P = 0·000002 and P = 0·0003, respectively) were replicated in the Caerphilly study, in addition to the association with LDL-C (P = 0·0004 and P = 0·001, respectively). In the Caerphilly study, interaction between fat (% energy) and rs328 at LPL on triacylglycerol (P = 0·02) and fat (% energy) and APOE haplotype on total cholesterol (P = 0·03) were observed; however, these interactions were not statistically significant after correction for multiple testing. In summary, we have shown that genetic variations at the APOE gene influence plasma lipid concentrations; however, the gene-diet interactions on lipids require confirmation in another larger cohort. The knowledge of combined effect of genetic and dietary factors on lipid profile could help us to a better understanding of the pathogenesis in the CVD.

References

1. Musunuru, K (2010) Lipids 45, 907–14.Google Scholar
2. Shatwan, IM et al. (2016) Int J Mol Sci 17, 397.Google Scholar
3. Bennet, A.M et al. (2007) Jama 298, 1300–11.Google Scholar
4. Carvalho-Wells, AL et al. (2012) Am J Clin Nutr 96, 1447–53.Google Scholar
5. Nettleton, JA et al. (2007) Atherosclerosis 194, e131–40.CrossRefGoogle Scholar