Two New Immunogenetic Polymorphisms of the ApoB Gene and Their Effect on Serum Lipid Levels and Responses to Changes in Dietary Fat Intake

Ilmonen, Marja; Heliö, Tiina; Bütler, R.; Palotie, Aarno; Pietinen, Pirjo; Huttunen, Jussi K.; Tikkanen, Matti J.

doi:10.1161/01.atv.15.9.1287

Cited by 12 publications

(12 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In 102 healthy Finnish subjects, LDL cholesterol levels on a low-fat diet were higher in 10 men with an apo B 1896 (His-e-Arg) genotype than in men with His/His [114]. Compared with levels on a high fat, high cholesterol diet, there was a tendency to a reduced total cholesterol, LDL cholesterol, and apo B response in the men with His -> Arg.…”

Section: Diet Genetics and Coronary Artery Diseasementioning

confidence: 91%

Diet-gene interactions in human lipoprotein metabolism.

Dreon¹,

Krauss²

1997

Journal of the American College of Nutrition

View full text Add to dashboard Cite

Genetic variation can influence the effects of hypocholesterolemic dietary interventions on lipoproteins involved in coronary artery disease (CAD). Individuals with the E4 allelic variant of the apo E gene exhibit greater low-density lipoprotein (LDL) cholesterol reductions on low-fat, low-cholesterol diets than subjects with other alleles. Another apolipoprotein structural variant, apo A-IV-2, attenuates the response of LDL cholesterol to dietary cholesterol. Other studies have associated lipoprotein response to dietary modifications with DNA polymorphisms in the genes for apo B and the LDL receptor, and in the promoter region of the apo A-I gene. Studies in our laboratory involving variation in dietary fat and carbohydrate intake have demonstrated that alleles at the apo E gene locus are associated with changes in large, buoyant but not smaller, denser LDL subclasses. On the other hand, a low-fat diet induces a reduction in small, dense LDL in individuals with a genetically influenced metabolic profile characterized by a predominance of these particles. Moreover, reductions in LDL cholesterol and apo B in these subjects are greater than in the majority of subjects with larger LDL. Since in humans a predominance of small LDL signifies a higher risk for coronary artery disease than that associated with larger LDL, metabolic and genetic factors contributing to the small LDL trait may account for a substantial portion of the coronary risk benefit attributed to reduced-fat diets. Studies in large population groups or in suitable animal models will be necessary to determine the impact of genetic influences on dietary response affecting lipoprotein metabolism and their interactions with other environmental and hormonal factors.

show abstract

Section: Diet Genetics and Coronary Artery Diseasementioning

confidence: 91%

Diet-gene interactions in human lipoprotein metabolism.

Dreon¹,

Krauss²

1997

Journal of the American College of Nutrition

View full text Add to dashboard Cite

show abstract

“…The minor allele of BsrDI RFLP was also associated with an elevated REM. This polymorphism was recently described by Ilmonen et al 15 and causes an AAT to AGT change in codon 1887 (resulting in the substitution of arginine for serine). The loss of a basic amino acid could lead to changes in the apoB surface, including a charge change, as shown by the impaired immunoreactivity of LDL apoB with Mab D7.2.…”

Section: Védie Et Al November 1998mentioning

confidence: 87%

“…The loss of a basic amino acid could lead to changes in the apoB surface, including a charge change, as shown by the impaired immunoreactivity of LDL apoB with Mab D7.2. 15 The LDL REM was also associated with a variation at the apoCIII locus. There was a significant increase in LDL REM in carriers of the apoCIII SacI minor allele.…”

Section: Védie Et Al November 1998mentioning

confidence: 98%

“…32 All forms of polymorphism were typed by the polymerase chain reaction (PCR). DNA was analyzed for apoB restriction fragment length polymorphisms (RFLPs) with the endonuclease XbaI, EcoRI, MspI, RsaI, and BsrDI sites, all located in the coding region of the apoB gene, 14,15 and with the endonuclease SacI, HphI, MspI, and PstI sites in the 5Ј and 3Ј noncoding regions of the apoCIII and apoAI genes.…”

Section: Dna Analysismentioning

confidence: 99%

See 1 more Smart Citation

Charge Heterogeneity of LDL in Asymptomatic Hypercholesterolemic Men Is Related to Lipid Parameters and Variations in the ApoB and CIII Genes

Védie

Jeunemaı̂tre

Mégnien

et al. 1998

ATVB

View full text Add to dashboard Cite

Abstract-This study was carried out to examine the relationship between the charge on low density lipoproteins (LDLs) and lipid and clinical parameters in 104 asymptomatic dyslipidemic men and to identify biochemical and genetic factors that could contribute to the charge variability of LDL. LDL charge heterogeneity was evaluated by relative electrophoretic mobility (REM) on preformed 0.5% agarose gels and by chromatographic quantification of a minor electronegative LDL subfraction designated LDL(Ϫ were not due to oxidation, as measured by the lag phase and binding to the LDL receptor. The results of the 2 methods used to measure LDL charge were significantly correlated and had some identical characteristics (eg, association with LDL apoCIII content and plasma triglyceride levels in borderline and IIb dyslipidemic subjects); these methods reflect different specific features of LDL charge. The percentage of LDL(Ϫ) was correlated positively with the LDL sialic acid content (PϽ0.0001), whereas the REM was related to at least 2 distinct chromosomal loci. Multiple logistic analysis showed that individuals carrying minor alleles of BsrDI (PϽ0.05), apoCIII/SacI (PϽ0.01), as well as the frequent allele of XbaI (PϽ0.05) at the apoB and CIII gene loci had high REMs. This result suggests that LDL charge heterogeneity, which is positively correlated with the atherogenic lipid profile, is influenced by both genetic and biochemical factors.

show abstract

“…The latter underlies a restriction fragment length polymorphism detectable by the restriction enzyme XbaI . Also the four missense mutations 5869G (Ilmonen et al 1995), 5896G (Ilmonen et al 1995), 8344T (Huang et al 1990) and 10422C (Chen et al 1986) have previously been published, whereas missense mutation 11889A is a novel mutation.…”

Section: Discussionmentioning

confidence: 99%

Screening for mutations of the apolipoprotein B gene causing hypocholesterolemia

Leren¹,

Bakken²,

Hoel³

et al. 1998

Human Genetics

View full text Add to dashboard Cite

In this study we have performed analyses of apolipoprotein (apo) B at both the protein and gene level to search for mutations of the apoB gene causing hypocholesterolemia among 71 Norwegian subjects. None of the subjects possessed apoB of abnormal molecular weight as determined by SDS-polyacrylamide gel electrophoresis of lipoproteins in the 1.025 g/ml-1.063 g/ml density range. Screening for mutations in exon 26 of the apoB gene by analysis of single-strand conformation polymorphisms followed by DNA sequencing, revealed seven point mutations of which one is a novel mutation. Five of the mutations were missense mutations and two were sense mutations. A group of 143 hypercholesterolemic, nonfamilial hypercholesterolemia subjects served as a control group for comparisons of gene frequencies. The only statistically significant finding was that mutation 8344T at codon 2712 was more common among those with hypocholesterolemia. This finding is in accord with previous reports.

show abstract

Two New Immunogenetic Polymorphisms of the ApoB Gene and Their Effect on Serum Lipid Levels and Responses to Changes in Dietary Fat Intake

Cited by 12 publications

References 54 publications

Diet-gene interactions in human lipoprotein metabolism.

Diet-gene interactions in human lipoprotein metabolism.

Charge Heterogeneity of LDL in Asymptomatic Hypercholesterolemic Men Is Related to Lipid Parameters and Variations in the ApoB and CIII Genes

Screening for mutations of the apolipoprotein B gene causing hypocholesterolemia

Contact Info

Product

Resources

About