Abstract

The apolipoprotein E (APOE) polymorphism impacts blood lipids and biomarkers of oxidation and inflammation, contributing to an isoform-dependent disease risk. We investigated the effect of the APOE genotype on postprandial metabolism after consumption of three different isoenergetic (4200 kJ) meals in older adults with a CVD risk phenotype. In a randomized crossover study, participants with metabolic syndrome traits (APOE E3, n = 39; E4, n = 10; mean age, 70 ± 5 years; BMI 31.3 ± 3.0 kg/m2) consumed a Western-like diet high-fat (WDHF), Western-like diet high-carbohydrate (WDHC), or Mediterranean-like diet (MED) meal. Parameters of lipid and glucose metabolism, inflammatory, and oxidative parameters were analyzed in blood samples collected at fasting and 1–5 h postprandially. Data were analyzed by linear mixed models. The magnitude of the IL-6 increase after the WDHF meal was significantly higher in E4 than in E3 carriers (iAUC: E4 = 7.76 vs. E3 = 2.81 pg/mL × h). The time to detect the IL-6 increase was shorter in the E4 group. All meals produced postprandial glycemia, insulinemia, and lipidemia, without differences between the E3 and the E4 groups. IL-1β and oxidized LDL levels did not change postprandially. In conclusion, APOE E4 carriers display increased postprandial inflammation, indicated by higher postprandial IL-6 increase, when compared to non-carriers.

Highlights

  • The apolipoprotein E (APOE) genotype is an established risk factor for cardiovascular disease (CVD), neuropathology, and Alzheimer’s disease [1,2,3]

  • Discussion risk, this study examined for the first time the impact of the APOE genotype (E4 vs. E3)

  • The major finding was that the APOE genotype influences the postprandial IL-6 response, with carriers of the ε4 allele (E4 group) displaying markedly higher plasma IL-6 concentrations than ε3/ε3 individuals (E3 group) after the consumption of a Western-like diet high-fat (WDHF) meal

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Summary

Introduction

The apolipoprotein E (APOE) genotype is an established risk factor for cardiovascular disease (CVD), neuropathology, and Alzheimer’s disease [1,2,3]. ApoE is expressed as three different isoforms (E2, E3, and E4) that arise from three different alleles (ε2, ε3, and ε4, respectively), which are present with in varying frequency of 4.0/). The APOE4 carrier status is predictive of CVD and Alzheimer’s disease [1,2,3]. The pathological associations of APOE4 have been investigated widely, the main etiological mechanisms have not been clearly defined. The protein apoE is involved in multiple biological pathways and processes, including lipoprotein metabolism and intracellular cholesterol utilization [4,5], immunoregulation [6],

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