Influence of APOE-2 genotype on the relation between adiposity and plasma lipid levels in patients with vascular disease
Background: Apolipoprotein E ( APOE ) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotyp...
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| Veröffentlicht in: | International Journal of Obesity Jg. 39; H. 2; S. 265 - 269 |
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| Hauptverfasser: | , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
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Nature Publishing Group UK
01.02.2015
Nature Publishing Group |
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| ISSN: | 0307-0565, 1476-5497, 1476-5497 |
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| Abstract | Background:
Apolipoprotein E (
APOE
) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the
APOE
genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in ɛ2 homo- and heterozygote patients.
Methods:
This prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The
APOE
genotype was measured in all patients and revealed 58 ɛ2 homozygotes, 663 ɛ2 heterozygotes, 3181 ɛ3 homozygotes and 1548 ɛ4 carriers. The main dependent variable was non-high-density lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression.
Results:
There was significant effect modification by the
APOE
genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in ɛ2 homozygotes (
β
0.173, 95% confidence interval (CI) 0.031–0.314,
P
=0.018) and ɛ4 carriers (
β
0.033, 95% CI 0.020–0.046,
P
<0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in ɛ2 homozygotes (waist
β
0.063, 95% CI 0.015–0.110,
P
=0.011; VAT
β
0.580, 95% CI 0.270–0.889,
P
=0.001; MetS
β
1.760, 95% CI 0.668–2.852,
P
=0.002). Determinants of DBL in ɛ2 homo- and heterozygotes were VAT and MetS.
Conclusion:
The
APOE
genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in ɛ2 homozygote patients. Abdominal fat and MetS are determinants of DBL. |
|---|---|
| AbstractList | BACKGROUND: Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ζ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in ζ2 homo- and heterozygote patients. METHODS: This prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The APOE genotype was measured in all patients and revealed 58 ζ2 homozygotes, 663 ζ2 heterozygotes, 3181 ζ3 homozygotes and 1548 ζ4 carriers. The main dependent variable was non-highdensity lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression. RESULTS: There was significant effect modification by the APOE genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in ζ2 homozygotes (β 0.173, 95% confidence interval (CI) 0.031-0.314, P = 0.018) and ζ4 carriers (β 0.033, 95% CI 0.020-0.046, P < 0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in ζ2 homozygotes (waist β 0.063, 95% CI 0.015-0.110, P = 0.011; VAT β 0.580, 95% CI 0.270-0.889, P = 0.001; MetS β 1.760, 95% CI 0.668-2.852, P = 0.002). Determinants of DBL in ζ2 homo- and heterozygotes were VAT and MetS. CONCLUSION: The APOE genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in ζ2 homozygote patients. Abdominal fat and MetS are determinants of DBL. International Journal of Obesity (2015) 39, 265-269; doi: 10.1038/ijo.2014.105 Background:Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO [varepsilon]2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in [varepsilon]2 homo- and heterozygote patients.Methods:This prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The APOE genotype was measured in all patients and revealed 58 [varepsilon]2 homozygotes, 663 [varepsilon]2 heterozygotes, 3181 [varepsilon]3 homozygotes and 1548 [varepsilon]4 carriers. The main dependent variable was non-high-density lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression.Results:There was significant effect modification by the APOE genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in [varepsilon]2 homozygotes (β 0.173, 95% confidence interval (CI) 0.031-0.314, P=0.018) and [varepsilon]4 carriers (β 0.033, 95% CI 0.020-0.046, P<0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in [varepsilon]2 homozygotes (waist β 0.063, 95% CI 0.015-0.110, P=0.011; VAT β 0.580, 95% CI 0.270-0.889, P=0.001; MetS β 1.760, 95% CI 0.668-2.852, P=0.002). Determinants of DBL in [varepsilon]2 homo- and heterozygotes were VAT and MetS.Conclusion:The APOE genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in [varepsilon]2 homozygote patients. Abdominal fat and MetS are determinants of DBL. Background: Apolipoprotein E ( APOE ) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in ɛ2 homo- and heterozygote patients. Methods: This prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The APOE genotype was measured in all patients and revealed 58 ɛ2 homozygotes, 663 ɛ2 heterozygotes, 3181 ɛ3 homozygotes and 1548 ɛ4 carriers. The main dependent variable was non-high-density lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression. Results: There was significant effect modification by the APOE genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in ɛ2 homozygotes ( β 0.173, 95% confidence interval (CI) 0.031–0.314, P =0.018) and ɛ4 carriers ( β 0.033, 95% CI 0.020–0.046, P <0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in ɛ2 homozygotes (waist β 0.063, 95% CI 0.015–0.110, P =0.011; VAT β 0.580, 95% CI 0.270–0.889, P =0.001; MetS β 1.760, 95% CI 0.668–2.852, P =0.002). Determinants of DBL in ɛ2 homo- and heterozygotes were VAT and MetS. Conclusion: The APOE genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in ɛ2 homozygote patients. Abdominal fat and MetS are determinants of DBL. Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in ɛ2 homo- and heterozygote patients.BACKGROUNDApolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in ɛ2 homo- and heterozygote patients.This prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The APOE genotype was measured in all patients and revealed 58 ɛ2 homozygotes, 663 ɛ2 heterozygotes, 3181 ɛ3 homozygotes and 1548 ɛ4 carriers. The main dependent variable was non-high-density lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression.METHODSThis prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The APOE genotype was measured in all patients and revealed 58 ɛ2 homozygotes, 663 ɛ2 heterozygotes, 3181 ɛ3 homozygotes and 1548 ɛ4 carriers. The main dependent variable was non-high-density lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression.There was significant effect modification by the APOE genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in ɛ2 homozygotes (β 0.173, 95% confidence interval (CI) 0.031-0.314, P=0.018) and ɛ4 carriers (β 0.033, 95% CI 0.020-0.046, P<0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in ɛ2 homozygotes (waist β 0.063, 95% CI 0.015-0.110, P=0.011; VAT β 0.580, 95% CI 0.270-0.889, P=0.001; MetS β 1.760, 95% CI 0.668-2.852, P=0.002). Determinants of DBL in ɛ2 homo- and heterozygotes were VAT and MetS.RESULTSThere was significant effect modification by the APOE genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in ɛ2 homozygotes (β 0.173, 95% confidence interval (CI) 0.031-0.314, P=0.018) and ɛ4 carriers (β 0.033, 95% CI 0.020-0.046, P<0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in ɛ2 homozygotes (waist β 0.063, 95% CI 0.015-0.110, P=0.011; VAT β 0.580, 95% CI 0.270-0.889, P=0.001; MetS β 1.760, 95% CI 0.668-2.852, P=0.002). Determinants of DBL in ɛ2 homo- and heterozygotes were VAT and MetS.The APOE genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in ɛ2 homozygote patients. Abdominal fat and MetS are determinants of DBL.CONCLUSIONThe APOE genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in ɛ2 homozygote patients. Abdominal fat and MetS are determinants of DBL. Background:Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in ɛ2 homo- and heterozygote patients.Methods:This prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The APOE genotype was measured in all patients and revealed 58 ɛ2 homozygotes, 663 ɛ2 heterozygotes, 3181 ɛ3 homozygotes and 1548 ɛ4 carriers. The main dependent variable was non-high-density lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression.Results:There was significant effect modification by the APOE genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in ɛ2 homozygotes (β 0.173, 95% confidence interval (CI) 0.031–0.314, P=0.018) and ɛ4 carriers (β 0.033, 95% CI 0.020–0.046, P<0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in ɛ2 homozygotes (waist β 0.063, 95% CI 0.015–0.110, P=0.011; VAT β 0.580, 95% CI 0.270–0.889, P=0.001; MetS β 1.760, 95% CI 0.668–2.852, P=0.002). Determinants of DBL in ɛ2 homo- and heterozygotes were VAT and MetS.Conclusion:The APOE genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in ɛ2 homozygote patients. Abdominal fat and MetS are determinants of DBL. Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called dysbetalipoproteinemia (DBL). A possible predisposing factor for DBL is adiposity. We evaluated whether and to what extent the APOE genotype modifies the relation between adiposity and lipids in patients with manifest arterial disease and we looked at possible determinants of DBL in ɛ2 homo- and heterozygote patients. This prospective cohort study was performed in 5450 patients with manifest arterial disease from the Secondary Manifestations of ARTerial disease (SMART) study. The APOE genotype was measured in all patients and revealed 58 ɛ2 homozygotes, 663 ɛ2 heterozygotes, 3181 ɛ3 homozygotes and 1548 ɛ4 carriers. The main dependent variable was non-high-density lipoprotein cholesterol (non-HDL-c). The relation between adiposity (including body mass index (BMI), waist circumference (waist), visceral adipose tissue (VAT) and metabolic syndrome (MetS)) and lipids was evaluated with linear regression analyses. Determinants of DBL were evaluated using logistic regression. There was significant effect modification by the APOE genotype on the relation between non-HDL-c and BMI, waist, VAT and MetS. There was an association between BMI and non-HDL-c in ɛ2 homozygotes (β 0.173, 95% confidence interval (CI) 0.031-0.314, P=0.018) and ɛ4 carriers (β 0.033, 95% CI 0.020-0.046, P<0.001). In all genotypes, there was an effect of waist, VAT and MetS on non-HDL-c, but these effects were most distinct in ɛ2 homozygotes (waist β 0.063, 95% CI 0.015-0.110, P=0.011; VAT β 0.580, 95% CI 0.270-0.889, P=0.001; MetS β 1.760, 95% CI 0.668-2.852, P=0.002). Determinants of DBL in ɛ2 homo- and heterozygotes were VAT and MetS. The APOE genotype modifies the relation between adiposity and plasma lipid levels in patients with vascular disease. The relation between adiposity and lipids is present in all patients, but it is most distinct in ɛ2 homozygote patients. Abdominal fat and MetS are determinants of DBL. International Journal of Obesity (2015) 39, 265-269; doi: 10.1038/ijo.2014.105 |
| Audience | Academic |
| Author | van der Graaf, Y Visseren, F L J Asselbergs, F W Koopal, C Westerink, J |
| Author_xml | – sequence: 1 givenname: C surname: Koopal fullname: Koopal, C organization: Department of Vascular Medicine, University Medical Center Utrecht – sequence: 2 givenname: Y surname: van der Graaf fullname: van der Graaf, Y organization: Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht – sequence: 3 givenname: F W surname: Asselbergs fullname: Asselbergs, F W organization: Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, Durrer Center for Cardiogenetic Research, ICIN-Netherlands Heart Institute, Faculty of Population Health Sciences, Institute of Cardiovascular Science, University College London – sequence: 4 givenname: J surname: Westerink fullname: Westerink, J organization: Department of Vascular Medicine, University Medical Center Utrecht – sequence: 5 givenname: F L J surname: Visseren fullname: Visseren, F L J email: F.L.J.Visseren@umcutrecht.nl organization: Department of Vascular Medicine, University Medical Center Utrecht |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24946908$$D View this record in MEDLINE/PubMed |
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| Copyright | Macmillan Publishers Limited 2015 COPYRIGHT 2015 Nature Publishing Group Copyright Nature Publishing Group Feb 2015 Macmillan Publishers Limited 2015. |
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| DOI | 10.1038/ijo.2014.105 |
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The EARS Study. 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| Snippet | Background:
Apolipoprotein E (
APOE
) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder... Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called... BACKGROUND: Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ζ2 genotype can develop a disorder called... International Journal of Obesity (2015) 39, 265-269; doi: 10.1038/ijo.2014.105 Background:Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO [varepsilon]2 genotype can develop a... Background:Apolipoprotein E (APOE) genotypes are associated with different plasma lipid levels. People with the APO ɛ2 genotype can develop a disorder called... |
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| SubjectTerms | 631/208/205 692/308/174 692/699/2743/393 692/699/75/2099 692/699/75/593 Abdomen Adipose tissue Adiposity - genetics Analysis Apolipoprotein E Apolipoprotein E2 - genetics Apolipoprotein E2 - metabolism Apolipoproteins Blood circulation disorders Blood lipids Body fat Body Fat Distribution Body Mass Index Body size Cardiovascular disease Causes of Cholesterol Cohort analysis Complications and side effects Confidence intervals Dependent variables Epidemiology Evaluation Female Genetic aspects Genetic Predisposition to Disease - genetics Genotype Genotype & phenotype Genotypes Health Promotion and Disease Prevention Health risk assessment Health sciences Heterozygotes High density lipoprotein Homozygotes Humans Hyperlipoproteinemia Type III - genetics Hyperlipoproteinemia Type III - metabolism Hyperlipoproteinemia Type III - physiopathology Internal Medicine Lipid metabolism Lipids Lipids - blood Lipids - genetics Lipoproteins Male Medicine Medicine & Public Health Metabolic Diseases Metabolic disorders Metabolic syndrome Metabolic Syndrome - genetics Metabolic Syndrome - metabolism Middle Aged Obesity Obesity, Abdominal - genetics Obesity, Abdominal - metabolism original-article Patients Physiological aspects Plasma Prospective Studies Public Health Regression analysis Statistical analysis Vascular diseases Vascular Diseases - genetics Vascular Diseases - metabolism Vascular Diseases - physiopathology Vein & artery diseases |
| Title | Influence of APOE-2 genotype on the relation between adiposity and plasma lipid levels in patients with vascular disease |
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