Decreased HDL2 and HDL3 cholesterol, Apo A-I and Apo A-II, and increased risk of myocardial infarction.

Buring, Julie E.; O’Connor, Gerald T.; Goldhaber, Samuel Z.; Rosner, Bernard; Herbert, Peter N.; Blum, Conrad B.; Breslow, Jan L.; Hennekens, Charles H.

doi:10.1161/01.cir.85.1.22

Cited by 188 publications

(73 citation statements)

References 38 publications

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“…10,13 Studies of the genetic determination of apoA-I have found evidence of 1 major locus, 66 2 major loci, 67 or polygenes alone 68,69 influencing the variation in different populations. The LOD score of 2.02 at 128 cM in the present study suggests that variation in plasma apoA-I may be influenced by a gene on chromosome 12q.…”

Section: Klos Et Al Genome-wide Linkage Analyses 975mentioning

confidence: 99%

Genome-Wide Linkage Analysis Reveals Evidence of Multiple Regions That Influence Variation in Plasma Lipid and Apolipoprotein Levels Associated With Risk of Coronary Heart Disease

Klos

Kardia

Ferrell

et al. 2001

ATVB

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Abstract-Results of genome-wide linkage analyses to identify chromosomal regions that influence interindividual variation in plasma lipid and apolipoprotein levels in the Rochester, Minn, population are reported. Analyses were conducted for total cholesterol (total-C), triglycerides (TGs), high density lipoprotein cholesterol (HDL-C), apolipoprotein A-I, apolipoprotein A-II, apolipoprotein B, apolipoprotein C-II, apolipoprotein C-III, apolipoprotein E, the total-C/HDL-C ratio, and the TG/HDL-C ratio. Genotypes were measured for 373 genome-wide marker loci on 1484 individuals distributed among 232 multigeneration pedigrees sampled without regard to health status. LOD scores and estimates of additive genetic variance associated with map locations were obtained by using the variance-component method of linkage analysis. No evidence of linkage with genes influencing variation in age served as a negative control.Plasma apolipoprotein E levels and the apolipoprotein E gene served as a positive control (LOD score 4.20). Evidence (LOD score Ͼ2.00) was provided that was suggestive of a gene or genes on chromosomes 4 and 5 influencing variation in the apolipoprotein A-II level, on chromosome 12 influencing variation in the apolipoprotein A-I level, and on chromosome 17 influencing variation of total-C/HDL-C. These analyses provide new information about genomic regions in humans that influence interindividual variation in plasma lipid and apolipoprotein levels and serve as a basis for further fine-mapping studies to identify new genes involved in lipid metabolism.

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Section: Klos Et Al Genome-wide Linkage Analyses 975mentioning

confidence: 99%

Genome-Wide Linkage Analysis Reveals Evidence of Multiple Regions That Influence Variation in Plasma Lipid and Apolipoprotein Levels Associated With Risk of Coronary Heart Disease

Klos

Kardia

Ferrell

et al. 2001

ATVB

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“…ApoA-I is the major structural and regulatory protein of HDL and, like HDL, is higher in women than in men, 41 and is lower in patients with myocardial infarction 42 and coronary artery disease. 43 .…”

Section: Walden Et Al Hdl Andmentioning

confidence: 99%

“…Low HDL-C and HDL 2 -C are independent risk factors for CVD in cross-sectional prospective studies. [15][16][17][18][19]42,44,45 HDL-C and HDL 2 -C levels are higher in women compared with men, which is an inverse of the lower age-adjusted rates for coronary disease in women compared with men. [11][12][13][14]41 The observed HDL-C and HDL 2 -C reductions with the Step II diet are not small when viewed from the standpoint of the baseline differences between women and men.…”

Section: Walden Et Al Hdl Andmentioning

confidence: 99%

Differential Effect of National Cholesterol Education Program (NCEP) Step II Diet on HDL Cholesterol, Its Subfractions, and Apoprotein A-I Levels in Hypercholesterolemic Women and Men After 1 Year

Walden

Retzlaff

Buck

et al. 2000

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Abstract-We previously reported that high density lipoprotein cholesterol (HDL-C) decreases more in hypercholesterolemic (HC) women than in HC men ingesting an National Cholesterol Education Program (NCEP)Step II diet for 6 months. We examined these subjects to determine whether the differential HDL-C reduction persists after 12 months and whether it is associated with decreased HDL 2 -C and apoprotein A-I. Subjects were screened from an industrial workforce and were defined as HC if 2 low density lipoprotein cholesterol measurements were Ն75th percentile or defined as combined hyperlipidemic (CHL) if triglycerides were also Ն75th percentile. The subjects were then taught the NCEP Step II diet in 8 weekly classes and counseled quarterly. Seventy-three HC and 92 CHL women (mean ages 43 and 44 years, respectively) and 112 HC and 106 CHL men (ages 45 and 41 years, respectively) were studied. All groups reported similar total fat (24% to 26% kcal) and saturated fat (7.1% to 7.9% kcal) intakes at 1 year. HDL-C decreased 7.6% in HC women (PϽ0.01), exceeding the nonsignificant 1.3% decrease in HC men (Pϭ0.000). HDL 2 -C decreased 16.7% in HC women (PϽ0.01) compared with the nonsignificant 0.5% increase in HC men (Pϭ0.000). In CHL women and men, HDL-C decreased 3.5% and 3.9% (both PϽ0.01); HDL 2 -C decreased more in women (7.1%, PϽ0.01) than in men (4.3%, a nonsignificant difference). Apoprotein A-I decreased significantly (5.3%, PϽ0.01) in HC women only. Plasma triglycerides were unchanged. Low density lipoprotein cholesterol and weight changes were not different among the 4 groups. HDL-C, HDL 2 -C, and apoprotein A-I levels decreased more in HC women than in HC men after following the NCEP Step II diet for 1 year, continuing a trend observed with HDL-C at 6 months. The total HDL-C and HDL 2 -C reductions narrow the baseline differences between men and women by 50%. Whether this reduction impacts women's protection from cardiovascular disease deserves future study. Nonetheless, the results point to sex-based differences in intrahepatic glucose and fatty acid metabolism linked to alterations in HDL formation and removal. Key Words: hypercholesterolemia Ⅲ combined hyperlipidemia Ⅲ HDL cholesterol Ⅲ apoA-I Ⅲ low fat diet H eart disease is the most common cause of death in women and men in the United States. 1 Hypercholesterolemia is a major modifiable cardiovascular disease (CVD) risk factor in both sexes. [2][3][4] Dietary modification to lower LDL cholesterol (LDL-C) is the primary strategy for the population-based reduction in CVD risk. 5,6 The National Cholesterol Education Program (NCEP) recommends reducing saturated fat intake in 2 steps, to Ͻ10% of calories (step I) and Ͻ7% of calories (step II), in the initial management of individuals with hypercholesterolemia, regardless of sex, before instituting pharmacological measures. 6 Recently, we reported sex-equivalent reductions in LDL-C but significantly greater HDL cholesterol (HDL-C) reductions in hypercholesterolemic (HC) women compared with men 6 months after inst...

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“…inverse relationship between plasma APOA2 concentrations and cardiovascular disease (CVD) risk (2,3 ), findings of subsequent studies did not reveal significant associations or even suggest a proatherogenic role (4 -6 ).…”

mentioning

confidence: 95%

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

et al. 2007

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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>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.

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Decreased HDL2 and HDL3 cholesterol, Apo A-I and Apo A-II, and increased risk of myocardial infarction.

Abstract: Background. A large and consistent body of evidence supports thejudgment that elevation of total plasma blood cholesterol is a cause of myocardial infarction (MI)

Cited by 188 publications

References 38 publications

Genome-Wide Linkage Analysis Reveals Evidence of Multiple Regions That Influence Variation in Plasma Lipid and Apolipoprotein Levels Associated With Risk of Coronary Heart Disease

Genome-Wide Linkage Analysis Reveals Evidence of Multiple Regions That Influence Variation in Plasma Lipid and Apolipoprotein Levels Associated With Risk of Coronary Heart Disease

Differential Effect of National Cholesterol Education Program (NCEP) Step II Diet on HDL Cholesterol, Its Subfractions, and Apoprotein A-I Levels in Hypercholesterolemic Women and Men After 1 Year

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

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Decreased HDL2 and HDL3 cholesterol, Apo A-I and Apo A-II, and increased risk of myocardial infarction.

Abstract: Background. A large and consistent body of evidence supports thejudgment that elevation of total plasma blood cholesterol is a cause of myocardial infarction (MI)

Cited by 188 publications

References 38 publications

Genome-Wide Linkage Analysis Reveals Evidence of Multiple Regions That Influence Variation in Plasma Lipid and Apolipoprotein Levels Associated With Risk of Coronary Heart Disease

Genome-Wide Linkage Analysis Reveals Evidence of Multiple Regions That Influence Variation in Plasma Lipid and Apolipoprotein Levels Associated With Risk of Coronary Heart Disease

Differential Effect of National Cholesterol Education Program (NCEP) Step II Diet on HDL Cholesterol, Its Subfractions, and Apoprotein A-I Levels in Hypercholesterolemic Women and Men After 1 Year

The −256T&gt;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

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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