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  • 1
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    The −256T〉C Polymorphism in the Apolipoprotein A-II Gene Promoter Is Associated with Body Mass Index and Food Intake in the Genetics of Lipid Lowering Drugs and Diet Network Study
    Oxford University Press (OUP) ; 2007
    In:  Clinical Chemistry Vol. 53, No. 6 ( 2007-06-01), p. 1144-1152
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 53, No. 6 ( 2007-06-01), p. 1144-1152
    Abstract: Background: Apolipoprotein A-II (APOA2) plays an ambiguous role in lipid metabolism, obesity, and atherosclerosis. Methods: We studied the association between a functional APOA2 promoter polymorphism (−265T & gt;C) and plasma lipids (fasting and postprandial), anthropometric variables, and food intake in 514 men and 564 women who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. We obtained fasting and postprandial (after consuming a high-fat meal) measures. We measured lipoprotein particle concentrations by proton nuclear magnetic resonance spectroscopy and estimated dietary intake by use of a validated questionnaire. Results: We observed recessive effects for this polymorphism that were homogeneous by sex. Individuals homozygous for the −265C allele had statistically higher body mass index (BMI) than did carriers of the T allele. Consistently, after multivariate adjustment, the odds ratio for obesity in CC individuals compared with T allele carriers was 1.70 (95% CI 1.02–2.80, P = 0.039). Interestingly, total energy intake in CC individuals was statistically higher [mean (SE) 9371 (497) vs 8456 (413) kJ/d, P = 0.005] than in T allele carriers. Likewise, total fat and protein intakes (expressed in grams per day) were statistically higher in CC individuals (P = 0.002 and P = 0.005, respectively). After adjustment for energy, percentage of carbohydrate intake was statistically lower in CC individuals. These associations remained statistically significant even after adjustment for BMI. We found no associations with fasting lipids and only some associations with HDL subfraction distribution in the postprandial state. Conclusions: The −265T & gt;C polymorphism is consistently associated with food consumption and obesity, suggesting a new role for APOA2 in regulating dietary intake.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1373/clinchem.2006.084863
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2007
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  • 2
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    Erythrocyte Fatty Acid Composition and the Metabolic Syndrome: A National Heart, Lung, and Blood Institute GOLDN Study
    Oxford University Press (OUP) ; 2008
    In:  Clinical Chemistry Vol. 54, No. 1 ( 2008-01-01), p. 154-162
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 54, No. 1 ( 2008-01-01), p. 154-162
    Abstract: Background: Different fatty acids may vary in their effect on the metabolic syndrome (MetS). We tested whether fatty acid classes measured in erythrocytes are associated with the MetS or its components. Methods: Included were men [n = 497; mean (SD) age, 49 (16) years] and women [n = 539; age, 48 (16) years] from 187 families in a National Heart, Lung, and Blood Institute (NHLBI) family study of the Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) conducted in Utah and Minnesota. We used gas chromatography to measure erythrocyte fatty acids and obtained data on potential confounding variables from interviewer-administered questionnaires. Results: The prevalence of the MetS as defined by the updated Adult Treatment Panel III criteria was 36.8% in Utah and 39.6% in Minnesota (P & gt;0.05). In a multivariate model that included 4 fatty acid classes, covariates, and pedigree as a random effect, the odds ratios (95% confidence interval) for the MetS in the 1st, 2nd, 3rd, and 4th quartile of polyunsaturated fatty acids were 1.00, 0.72 (0.47–1.10), 0.67 (0.43–1.05), and 0.39 (0.24–0.64), respectively (P for trend = 0.0002). For the corresponding quartiles of saturated fatty acids, the odds ratios were 1.00, 1.19 (0.77–1.84), 1.48 (0.94–2.34), and 1.63 (1.01–2.63), respectively (P for trend = 0.03). Unlike n6 fatty acids, which showed an inverse association (P & lt;0.05) with MetS, n3, trans, and monounsaturated fatty acids were not associated with the MetS (P & gt;0.05). We observed significant correlations (P & lt;0.05) between fatty acid classes, insulin, and components of the MetS. Conclusions: Polyunsaturated fats are inversely associated with the MetS, whereas saturated fatty acids are positively associated with the MetS, probably through their effect on lipids, adiposity, insulin, and blood pressure.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1373/clinchem.2007.095059
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2008
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  • 3
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    Lipoprotein Lipase S447X variant associated with VLDL, LDL and HDL diameter clustering in the MetS
    Springer Science and Business Media LLC ; 2011
    In:  Lipids in Health and Disease Vol. 10, No. 1 ( 2011), p. 143-
    Details
    In: Lipids in Health and Disease, Springer Science and Business Media LLC, Vol. 10, No. 1 ( 2011), p. 143-
    Type of Medium: Online Resource
    ISSN: 1476-511X
    URL: Article
    DOI: 10.1186/1476-511X-10-143
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 2091381-3
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  • 4
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    Behavior related genes, dietary preferences and anthropometric traits
    Wiley ; 2017
    In:  The FASEB Journal Vol. 31, No. S1 ( 2017-04)
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    In: The FASEB Journal, Wiley, Vol. 31, No. S1 ( 2017-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v31.S1
    DOI: 10.1096/fasebj.31.1_supplement.299.1
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 5
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    Abstract 908: In Vivo Role of the Pharmacogenetics of Glucuronidation in the Disposition and Triglyceride Response to Fenofibrate
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Vol. 116, No. suppl_16 ( 2007-10-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 116, No. suppl_16 ( 2007-10-16)
    Abstract: In spite of optimal low-density lipoprotein (LDL-C) lowering with statins, cardiovascular risk remains high for patients with elevated triglyceride (TG)-low high-density cholesterol (HDL-C) profiles. Fenofibric acid, the active moiety of fenofibrate, acts on the peroxisome proliferator-activated nuclear receptor-alpha (PPAR-α) to lower TG and raise HDL-C. The extent of lipid response has been shown to be associated with serum concentrations (conc.) of fenofibric acid. In vitro work confirms fenofibric acid is primarily eliminated by UDP-glucuronosyltransferases (UGTs) including UGT2B7, and others (UGT1A1, UGT1A3 and UGT1A9). Therefore, we hypothesized genetic variations in UGT activity may be associated with fenofibric acid conc. and thus may influence lipid response. Purpose: To test if the A-327G SNP (rs7662029) for UGT2B7, which has been shown to modulate UGT2B7 expression in vitro, is associated with serum conc. of fenofibric acid and TG response in vivo . Methods: As part of the NHLBI sponsored Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study, participants providing consent and not currently taking lipid lowering medications, were analyzed for fasting lipid response pre and post 21 days of once daily 160mg fenofibrate. TG response was calculated by the log of the ratio of the average of the 2 pre- and post-fenofibrate exposure TG determinations. Associations between UGT2B7 A-327G genotype and steady-state trough fenofibric acid conc. as well as TG response were analyzed by linear regression. Results : 745 participants (51% male) with both genotype and phenotype data were included. The mean (SD) age was 49 (16) years and the median (25 th ,75 th percentile) % change in TG concentrations was -32.3 (−45.2, −19.0). The G allele frequency for UGT2B7A 〉 G was 0.49 and was in HWE (p = 0.8). After adjusting for age, age 2 , sex, alcohol use, height and serum creatinine, strong associations were observed between UGT2B7 A-327G genotypes and steady-state trough fenofibric acid conc. (log-transformed, p = 4 × 10 −8 ) as well as TG response (p = 0.002, also adjusted for baseline TG). Conclusion : This study suggests UGT2B7 A-327G genotype may contribute to TG response by way of influencing glucuronidation activity of fenofibric acid.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.116.suppl_16.II_178-a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1466401-X
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  • 6
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    Abstract P190: Genome-wide Association Study Suggests that Inflammation and Insulin Regulation Pathways May Mediate Lipoprotein Diameter Response to Fenofibrate
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 125, No. suppl_10 ( 2012-03-13)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. suppl_10 ( 2012-03-13)
    Abstract: Shifts in lipoprotein diameter occur in insulin resistant (IR) patients - a known risk factor for cardiovascular disease. Fenofibrate modulates lipoprotein markers in a manner which is expected to reduce the risk of adverse cardiovascular events. However inter-individual variability in response to fenofibrate is very high. We aimed to examine phenotype-variant associations with shifts in lipoprotein diameter, for each of the three fractions of lipoprotein, in response to a three-week fenofibrate trial. Participants formed the general population sample from that Genetics of Lipid Lowering Drugs and Diet Network (n=817; mean age of 48.8 ± 16.2 y). Very-low, low- and high- density lipoprotein diameters were measured using NMR spectroscopy before and after a 3-week fenofibrate treatment (160mg/day). Lipoprotein diameter change, for each fraction, was calculated using growth curve models which modeled compliance with the fenofibrate protocol. Associations between single nucleotide polymorphisms on the Affymetrix 6.0 chip and lipoprotein diameter change were assessed using mixed linear models, adjusted for age, sex, study center, and family. A Bonferroni correction for multiple testing was used, with genome wide levels of significance set at P 〈 1.97*10 -08 . Given power problems inherent in using change scores, suggestive levels of significance were set at P 〈 1.97 * 10 -06 where there were more than five hits at this level within a 500kb region. The AHCLY2 ( P 〈 3.95*10 -08 ) gene was significantly associated with very-low density lipoprotein diameter. 14 genes reached suggestive levels of significance ( Table 1 ). We conclude that genes previously associated with inflammation ( LPAR1 , GRP110 ) and insulin ( PION , EIF2AK3 , CHRM3 , WNT ) may mediate lipoprotein diameter response to fenofibrate. Upon replication in clinical populations, this may help understand the co-occurrence of IR, inflammation and cardiovascular disease as well the mechanisms of action and therapeutic potential of fenofibrate's role in patients with IR. Table 1 Significant, and suggestive genotype-phenotype associations from a genome-wide study investigating genetic associations with VLDL, LDL and HDL diameter changes in response to fenofibrate Gene Response phenotype 1 P-value 2 Previous associations 3 AHCLY2 VLDL 3.95*10 -09 Produces an enzyme necessary for methylation DOCK4 VLDL 1.39*10 -07 - PPARG HDL 2.87*10 -07 Increases expression of ABCA1; target of thiazolidinediones used to treat insulin resistance ACCSL HDL 5.18*10 -07 - TFAP2A HDL 5.26*10 -07 cardiomyopathy PPTC7 HDL 6.40*10 -07 - NSUN3 HDL 6.45*10 -07 - RPLP1 HDL 6.47*10 -07 - ORK2 HDL 9.10*10 -07 Olfactory receptor G-protein coupled gene LPAR1 HDL 9.10*10 -07 inflammation, adipogenesis GPR110 VLDL 2.97*10 -06 G-protein coupled gene, inflammation EIF2AK3 VLDL 7.02*10 -06 insulin secretion, type 2 diabetes CHRM3 HDL 3.63*10 -06 insulin secretion, type 2 diabetes PLD1 VLDL 6.75*10 -06 insulin secretion and lipid droplet formation TINK VLDL 6.75*10 -06 wnt signaling, type 2 diabetes Abbreviations: VLDL: very-low density lipoprotein; LDL: low-density lipoprotein, HDL: High density lipoprotein 1 Diameter change 2 Smallest p-value for a single phenotype-variant association within the gene 3 PubMed searches for the genes where within the gene single nucleotide polymorphisms were associated at ( P 〈 1.97 * 10 -06 ).
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.125.suppl_10.AP190
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 7
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    Abstract P361: The First Genome-Wide Association Study (GWAS) of GlycA, an NMR-Derived Marker of Inflammation, Reveals Associations With a Variant in the Intron of TXNL4B Across Two Cohorts
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Vol. 131, No. suppl_1 ( 2015-03-10)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 131, No. suppl_1 ( 2015-03-10)
    Abstract: Markers of inflammation reflect metabolic dysfunction and may predict incident cardiovascular events. GlycA is a new NMR-derived plasma marker of inflammation. Our goal was to undertake first characterization of the genetic variants associated with fasting GlycA, to elucidate the pathways from genes to inflammation. We completed a GWAS in the Caucasian-ancestry population of The Multi-Ethnic Study of Atherosclerosis (MESA; N=2,520; 48% male, mean age 62.7 y). We specified linear regressions models with GlycA as the outcome, and ~2.5 million single nucleotide polymorphisms (SNPs) directly genotyped or imputed from HapMap as the predictors in separate models; all models additionally controlled for age, gender, alcohol intake (g/day), smoking status (yes / no) and 4 principal components of population structure. In MESA, 5 SNPs reached genome-wide levels of significance (P 〈 10 -8 ; Table 1). Forty six SNPs reached a ‘discovery threshold’ of P 〈 10 -5 in MESA, but only one (rs217181; minor allele frequency = .18) replicated in the Genetics of Lipid Lowering Drug Network (GOLDN; N=817; 48% male, mean age=48.8 years) after an FDR multiple testing correction. Rs217181 is located in the intron of TXNL4B , thioredoxin-like 4B, and in close proximity to HP , Haptoglobin , and HPR, Haptoglobin-related Protein . Rs217181 has been validated as associating with levels of haptoglobin protein. Haptoglobin is released by the liver and reduces hemoglobin’s oxidative activity. Our data suggests that rs217181 is involved in inflammation status, and may be a risk factor for adverse cardiovascular events. We would encourage replication of these findings in other cohorts, and are undertaking examination of this association in non-Caucasian individuals.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.131.suppl_1.p361
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
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  • 8
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    Abstract 141: APOA1, CETP, and CILP2 Variants Modify the Lipid Response to Fenofibrate: Genetics of Lipid Lowering and Diet Network
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 32, No. suppl_1 ( 2012-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. suppl_1 ( 2012-05)
    Abstract: Introduction: Despite the widespread use of fibrates in treatment of dyslipidemia, the observed response is highly heterogeneous, suggesting a role for genetic determinants. Whether replicated variants associated with blood lipids identified by genome wide association studies (GWAS) are also associated with lipid response to fenofibrate is unknown. Objectives: To test if 95 genome-wide significant loci identified in a recent meta-analysis of blood lipids are associated with changes in high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), non-HDL-C, and triglycerides (TG) following 3 weeks of therapy with 160 mg of micronized fenofibrate. Methods: Using data from 861 European American Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) participants, we fit mixed linear models with baseline blood lipids and the post-to-pre fenofibrate treatment ratio of blood lipid levels as outcomes, the corresponding genetic markers from the published meta-analysis as predictors, and age, sex, pedigree, and ancestry as assessed by principal components as covariates. A Bonferroni correction was applied to adjust for multiple comparisons. Least square means were used to report the direction of fenofibrate-induced changes by genotype. Results: We observed statistically significant associations between rs964184 , a variant near the APOA1 gene, and baseline HDL-C (P 〈 0.0001) and baseline TG (P 〈 0.0001), as well as with diminished response to fenofibrate as evidenced by a smaller increase in HDL-C (P 〈 0.0001) and a smaller decrease in TG (P=0.0001) per each copy of the variant allele. Additionally, we report suggestive associations of rs3764261 locus in the CETP gene and the rs10401969 locus in the CILP2 gene with decreased fenofibrate response as measured by changes in LDL-C (P=0.0003 and 0.02, respectively) and non-HDL-C (P=0.004 and 0.005, respectively). Conclusions: We have identified several novel biologically relevant loci associated with baseline blood lipids and fenofibrate-induced changes in blood lipids.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.32.suppl_1.A141
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1494427-3
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  • 9
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    High-fat meal effect on LDL, HDL, and VLDL particle size and number in the Genetics of Lipid-Lowering drugs and diet network (GOLDN): an interventional study
    Springer Science and Business Media LLC ; 2011
    In:  Lipids in Health and Disease Vol. 10, No. 1 ( 2011-12)
    Details
    In: Lipids in Health and Disease, Springer Science and Business Media LLC, Vol. 10, No. 1 ( 2011-12)
    Abstract: Postprandial lipemia (PPL) is likely a risk factor for cardiovascular disease but these changes have not been well described and characterized in a large cohort. We assessed acute changes in the size and concentration of total and subclasses of LDL, HDL, and VLDL particles in response to a high-fat meal. Participants (n = 1048) from the Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) Study who ingested a high-fat meal were included in this analysis. Lipids were measured at 0 hr (fasting), 3.5 hr, and 6 hr after a standardized fat meal. Particle size distributions were determined using nuclear magnetic resonance spectroscopy. Analyses were stratified by baseline triglycerides (normal vs. elevated) and gender. The effect of PPL on changes in lipoprotein subclasses was assessed using repeated measures ANOVA. Results Postprandially, LDL-C, HDL-C, VLDL-C, and triglycerides increased regardless of baseline triglyceride status, with the largest increases in VLDL-C and TG; however, those with elevated triglycerides demonstrated larger magnitude of response. Total LDL particle number decreased over the 6-hour time interval, mostly from a decrease in the number of small LDL particles. Similarly, total VLDL particle number decreased due to reductions in medium and small VLDL particles. Large VLDL particles and chylomicrons demonstrated the largest increase in concentration. HDL particles demonstrated minimal overall changes in total particle number. Conclusions We have characterized the changes in LDL and VLDL particle number, and their subclass patterns following a high-fat meal.
    Type of Medium: Online Resource
    ISSN: 1476-511X
    URL: Article
    DOI: 10.1186/1476-511X-10-181
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
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  • 10
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    Genetic variants in human CLOCK associate with total energy intake and cytokine sleep factors in overweight subjects (GOLDN population)
    Springer Science and Business Media LLC ; 2010
    In:  European Journal of Human Genetics Vol. 18, No. 3 ( 2010-3), p. 364-369
    Details
    In: European Journal of Human Genetics, Springer Science and Business Media LLC, Vol. 18, No. 3 ( 2010-3), p. 364-369
    Type of Medium: Online Resource
    ISSN: 1018-4813 , 1476-5438
    URL: Article
    DOI: 10.1038/ejhg.2009.176
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 2005160-8
    SSG: 12
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