Apolipoprotein E genotype and the cardiovascular disease risk phenotype: Impact of sex and adiposity (the FINGEN study)

Kofler, Barbara; Miles, Elizabeth A.; Curtis, Peter J.; Armah, Christopher K.; Tricon, Sabine; Grew, J P; Napper, Frances L.; Farrell, Leslie; Packard, Christopher J.; Mathers, John C.; Williams, Christine M.; Calder, Philip C.; Minihane, Anne Marie

doi:10.1016/j.atherosclerosis.2012.01.042

Cited by 34 publications

(43 citation statements)

References 14 publications

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“…In the present study, we observed that the plasma lipid and apolipoprotein responses to a fish oil intervention were influenced by sex [50]. In fact, plasma HDL-C levels increased after supplementation, but only in women.…”

Section: Discussionmentioning

confidence: 73%

Effects of Age, Sex, Body Mass Index and APOE Genotype on Cardiovascular Biomarker Response to an n-3 Polyunsaturated Fatty Acid Supplementation

Thifault¹,

Cormier²,

Bouchard-Mercier³

et al. 2013

Lifestyle Genomics

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Objectives: To test whether age, sex, body mass index (BMI), and the apolipoprotein E (APOE) genotype are associated with the metabolic response to an n-3 polyunsaturated fatty acid (PUFA) supplementation. Methods: 210 subjects followed a 2-week run-in period based on Canada's Food Guide and underwent a 6-week 5 g/day fish oil supplementation (1.9 g of eicosapentaenoic acid and 1.1 g of docosahexaenoic acid). Cardiovascular disease risk factors were measured. Results: n-3 PUFA supplementation was associated with a decrease of plasma triglyceride levels (p = 0.0002) as well as with an increase of fasting glucose (FG) levels (p = 0.02). Age was associated with post-intervention plasma total cholesterol (p = 0.01), low-density lipoprotein cholesterol (p = 0.007), apolipoprotein B (p = 0.04), and insulin (p = 0.002) levels. Sex was associated with post-intervention plasma high-density lipoprotein cholesterol levels (p = 0.02). BMI was associated with plasma FG (p = 0.02) and insulin levels (p < 0.0001) after the supplementation. APOE genotype was associated with FG (p = 0.001) and C-reactive protein levels (p = 0.03) after the supplementation. Conclusion: Results suggest that age, sex, BMI, and the APOE genotype contribute to the inter-individual variability observed in the metabolic response to an n-3 PUFA supplementation.

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Section: Discussionmentioning

confidence: 73%

Effects of Age, Sex, Body Mass Index and APOE Genotype on Cardiovascular Biomarker Response to an n-3 Polyunsaturated Fatty Acid Supplementation

Thifault¹,

Cormier²,

Bouchard-Mercier³

et al. 2013

Lifestyle Genomics

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“…In the population at large, the e2 and the e4 alleles have been linked to high triglyceride levels [19][20][21]31]. The LDL receptor recognises ApoE and ApoB-100 and plays a crucial role in cholesterol homeostasis [32], whereas the structurally related very LDL receptor recognises ApoE, but not ApoB-100, and plays an important role in triglyceride metabolism [33].…”

Section: Discussionmentioning

confidence: 99%

“…There are three common alleles of the APOE gene (e2, e3 and e4). Individuals carrying the e4 allele have higher total and LDL cholesterol levels than individuals with the commonest e3e3 genotype and those carrying the e2 allele have lower levels of total and LDL cholesterol [19][20][21]. In addition, associations between APOE genotype and triglycerides [18] and circulating apolipoprotein (Apo)E and ApoB concentrations have been reported in the general population [18,22,23].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, associations between APOE genotype and triglycerides [18] and circulating apolipoprotein (Apo)E and ApoB concentrations have been reported in the general population [18,22,23]. Taken together, e4 allele carriers represent the risky APOE genotype [19][20][21][22][23]. Nevertheless, the role of APOE gene polymorphisms in lipid metabolism disturbances in OSA, a condition known to be associated with increased cardiovascular risk, is unclear.…”

Section: Introductionmentioning

confidence: 99%

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Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea

et al. 2013

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There is increasing evidence that intermittent hypoxia resulting from obstructive sleep apnoea (OSA) is independently associated with dyslipidaemia. Currently, no data exist on potential links between OSA-related dyslipidaemia and susceptibility genes for dyslipidaemia in such patients. Our aim was to study the effects of the apolipoprotein E (APOE) genotype and sleep apnoea severity on atherogenic dyslipidaemia in patients with OSA.519 clinically stable subjects prospectively recruited at a tertiary referral teaching hospital underwent full polysomnography. APOE gene polymorphisms were assessed using real-time PCR.In all APOE genotype groups, serum triglycerides increased while high-density lipoprotein (HDL) cholesterol was reduced with increasing severity of OSA in each APOE genotype group, whereas the deleterious effects of OSA on serum apolipoprotein (Apo)B levels were observed in e2 carriers and the e3/e3 genotype only. Nevertheless, the e4 allele carriers had ApoB levels within the risk range, irrespective of nocturnal hypoxia. In addition, among patients with the high-risk e4 genotype, those with the most severe nocturnal hypoxia had significantly higher triglyceride and lower HDL cholesterol levels compared with nonhypoxic e4 subjects. APOE genotype and the oxygen desaturation index were both independent predictors of serum triglyceride levels (p50.009 and p,0.001, respectively; R 2 50.148) and ApoB levels (p50.001 and p50.003, respectively; R 2 50.104). Our findings suggest that OSA has adverse effects on several lipid parameters over and above the effects carried by APOE genotype. Further st1udies are needed to analyse the effects of high-risk genotypes on metabolic and cardiovascular outcomes in patients with OSA. @ERSpublications OSA has adverse effects on several lipid parameters in addition to the effects carried by the APOE genotype

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“…66 It should, however, be emphasized that even homozygosity for the ε-4 allele only partially accounts for vascular risk. 67 White matter pathology is frequently encountered in AD, being associated with focal symptomatology as well as global cognitive impairment. Aβ deposition in cortical and leptomeningeal arteries is strongly correlated with the APOE ε-4 allele, resulting in cerebral amyloid arteriopathy (CAA).…”

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confidence: 99%

Apolipoprotein E ε-4 as a genetic determinant of Alzheimer’s disease heterogeneity

Kotze¹,

Lückhoff²,

Brand³

et al. 2015

DNND

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Alzheimer's disease (AD) displays a high degree of heterogeneity in terms of its etiology, presentation, prognosis, and treatment response. This can partly be explained by highpenetrance mutations in the amyloid precursor protein, presenilin 1 and presenilin 2 genes causing amyloid beta aggregation, which is a major pathogenic mechanism in the development of earlyonset AD in a small subgroup of patients. Late-onset AD is considered a polygenic disorder in which cumulative risk resulting from interaction with modifiable environmental risk factors may be responsible for the majority of cases. The ε-4 allele of the apolipoprotein E (APOE) gene has emerged as the most significant genetic risk factor for late-onset AD, influencing nearly every pathogenic domain affected in AD. It is a major risk factor for cerebral amyloid angiopathy, recognized as a common pathological finding in an AD subtype associated with white matter dysfunction. The APOE ε-4 allele is also a known risk factor for ischemic stroke, which can result in vascular dementia or contribute to subcortical vascular dysfunction. In this review, we evaluate the clinical relevance of APOE genotyping in relation to cholesterol metabolism and available evidence on risk reduction strategies applicable to AD.

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Apolipoprotein E genotype and the cardiovascular disease risk phenotype: Impact of sex and adiposity (the FINGEN study)

Cited by 34 publications

References 14 publications

Effects of Age, Sex, Body Mass Index and APOE Genotype on Cardiovascular Biomarker Response to an n-3 Polyunsaturated Fatty Acid Supplementation

Effects of Age, Sex, Body Mass Index and APOE Genotype on Cardiovascular Biomarker Response to an n-3 Polyunsaturated Fatty Acid Supplementation

Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea

Apolipoprotein E ε-4 as a genetic determinant of Alzheimer’s disease heterogeneity

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Apolipoprotein E genotype and the cardiovascular disease risk phenotype: Impact of sex and adiposity (the FINGEN study)

Cited by 34 publications

References 14 publications

Effects of Age, Sex, Body Mass Index and APOE Genotype on Cardiovascular Biomarker Response to an n-3 Polyunsaturated Fatty Acid Supplementation

Effects of Age, Sex, Body Mass Index and APOE Genotype on Cardiovascular Biomarker Response to an n-3 Polyunsaturated Fatty Acid Supplementation

Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea

Apolipoprotein E &epsilon;-4 as a genetic determinant of Alzheimer&rsquo;s disease heterogeneity

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Apolipoprotein E ε-4 as a genetic determinant of Alzheimer’s disease heterogeneity