Abstract
Apolipoprotein (APO) E (ε) genotype is considered to play an important role in lipid responses to dietary fat manipulation but the impact on novel cardiometabolic risk markers is unclear. To address this knowledge gap, we investigated the relationship between the APOE genotype and cardiometabolic risk markers in response to acute and chronic dietary fat intakes. Associations with fasting (baseline) outcome measures (n = 218) were determined using data from the chronic DIVAS (n = 191/195 adults at moderate cardiovascular disease risk) and acute DIVAS-2 (n = 27/32 postmenopausal women) studies examining the effects of diets/meals varying in saturated, polyunsaturated and monounsaturated (MUFA) fatty acid composition. Participants were retrospectively genotyped for APOE (rs429358, rs7412). For baseline cardiometabolic outcomes, E4 carriers had higher fasting total and low-density lipoprotein-cholesterol (LDL-C), total cholesterol: high-density lipoprotein-cholesterol (HDL-C) and LDL-C: HDL-C ratios, but lower C-reactive protein (CRP) than E3/E3 and E2 carriers (p ≤ 0.003). Digital volume pulse stiffness index was higher in E2 carriers than the E3/E3 group (p = 0.011). Following chronic dietary fat intake, the significant diet × genotype interaction was found for fasting triacylglycerol (p = 0.010), with indication of a differential responsiveness to MUFA intake between the E3/E3 and E4 carriers (p = 0.006). Test fat × genotype interactions were observed for the incremental area under the curve for the postprandial apolipoprotein B (apoB; p = 0.022) and digital volume pulse reflection index (DVP-RI; p = 0.030) responses after the MUFA-rich meals, with a reduction in E4 carriers and increase in the E3/E3 group for the apoB response, but an increase in E4 carriers and decrease in the E3/E3 group for the DVP-RI response. In conclusion, baseline associations between the APOE genotype and fasting lipids and CRP confirm previous findings, although a novel interaction with digital volume pulse arterial stiffness was observed in the fasted state and differential postprandial apoB and DVP-RI responses after the MUFA-rich meals. The reported differential impact of the APOE genotype on cardiometabolic markers in the acute and chronic state requires confirmation.
Highlights
The apolipoprotein (APO) E (ε) genotype is the most widely researched single nucleotide polymorphism in relation to cardiovascular disease (CVD) risk, with the APOE4 allele linked with increased total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), CVD risk and mortality [1,2,3,4,5]
Important to investigate common single nucleotide polymorphisms related with CVD risk that impact on response to key population dietary fat recommendations for CVD risk reduction
This is the first data analysis that has examined both the chronic and acute impact of dietary fat manipulation on novel and established cardiometabolic risk markers according to the APOE genotype
Summary
The apolipoprotein (APO) E (ε) genotype is the most widely researched single nucleotide polymorphism in relation to cardiovascular disease (CVD) risk, with the APOE4 allele linked with increased total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), CVD risk and mortality [1,2,3,4,5]. Studies to date have focused on high-fat, high saturated fatty acid (SFA), low-fat and high-fat, high-SFA with fish oil interventions [6,7,8,9,10,11,12], whilst little is known of the interactions between the APOE genotype with n-6 polyunsaturated (PUFA) and monounsaturated (MUFA) fatty acid intakes. This is important and timely given that population dietary recommendations for CVD prevention advise the reduction of SFA intakes to ≤10% of total energy (%TE) via replacement with n-6 PUFA or MUFA. Endothelial dysfunction is recognised as a key modifiable event in coronary atherosclerosis, but limited data are available on the impact of APOE on the responsiveness of vascular reactivity to dietary fat composition [13]
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