Plasma lipoprotein lipids in relation to the MspI polymorphism of the apolipoprotein All gene in Caucasian men Lack of association with plasma triglyceride concentration

Rajput-Williams, J.; Eyre, Jeanette; Nanjee, M. Nazeem; Crook, David; Scott, James; Miller, N. E.

doi:10.1016/0021-9150(89)90006-3

Cited by 18 publications

(14 citation statements)

References 15 publications

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“…Studies in mice have shown that altered expression of apoAII influ- enced HDL levels (15) and aortic fatty streak development (30). However, various population studies (10)(11)(12)(13), as well as our present results, have failed to reveal significant relationships between apoAII gene polymorphisms and HDL levels in humans. In addition, studies ofindividuals homozygous for a mutation resulting in apoAII deficiency did not show any striking alterations in lipoprotein levels as compared to the average lipoprotein levels in the Japanese population (31).…”

Section: Discussioncontrasting

confidence: 53%

“…In each of the six studies, myocardial infarct patients had significantly lower apoAll levels than their matched controls, and in one study apoAll levels were the phenotype that was most discriminative of myocardial infarct survivors from their controls (3). Population studies of the apoAII gene that used a relatively uninformative Msp I restriction fragment length polymorphism have suggested possible associations with apoAII levels (8,(10)(11)(12) and triglyceride (TG) levels (13). Genetic studies in mice, involving naturally occurring variations and transgenic animals, have demonstrated important effects of the apoAll gene on lipoprotein metabolism and the development of preatherosclerotic fatty streak lesions (14,15).…”

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confidence: 99%

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Evidence for linkage of the apolipoprotein A-II locus to plasma apolipoprotein A-II and free fatty acid levels in mice and humans.

Warden

Daluiski

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Although it has been hypothesized that the synteny between mouse and human genes provides an approach to the localization of genes that determine quantitative traits in humans, this has yet to be demonstrated. We tested this approach with two quantitative traits, plasma apolipoprotein A-Il (apoAll) and free fatty acid (FFA) levels. ApoAII is the second most abundant protein of high density lipoprotein particles, but its function remains largely unknown. We now show that, in a backcross between strains Mus spretus and C57BL/6J, apoAII levels correlate with plasma FFA concentrations on both chow (P < 0.0001) and high-fat (P < 0.0003) diets and that apoAll levels are linked to the apoAII gene (P < 0.0002). To test whether variations of the apoAll gene influence plasma lipid metabolism in humans, we studied 306 individuals in 25 families enriched for coronary artery disease. The segregation of the apoAII gene was followed by using an informative simple sequence repeat in the second intron of the gene and two nearby genetic markers. Robust sib-pair linkage analysis was performed on members of these families using the SAGE linkage programs. The results suggest linkage between the human apoAll gene and a gene controlling plasma apoAII levels (P = 0.03). Plasma apoAII levels were also significantly correlated with plasma FFA levels (P = 0.007). Moreover, the apoAII gene exhibited linkage with a gene controlling FFA levels (P = 0.003). Evidence for nonrandom segregation was seen with markers as far as 6-12 centimorgans from the apoAll structural locus. These data provide evidence, in two species, that the apoAII gene is linked to a gene that controls plasma apoAll levels and that apoAII influences, by an unknown mechanism, plasma FFA levels. The results iliustrate the utility of animal studies for analysis of complex traits.

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Section: Discussioncontrasting

confidence: 53%

mentioning

confidence: 99%

Evidence for linkage of the apolipoprotein A-II locus to plasma apolipoprotein A-II and free fatty acid levels in mice and humans.

Warden

Daluiski

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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“…In the females, however, a similar trend was present. In contrast, Ferns et al [21] observed an excess of the Ml (3.0/3.0) genotype in hypertriglyceridemic patients at tending lipid clinics, which could not be con firmed in a later study [23]. These discrepan cies between different studies may be due to differences in ethnic origin, age, source and size of sample, or to differential expression of the gene.…”

Section: Resultscontrasting

confidence: 45%

“…Table 1 shows the distribution of apo A-II RFLP (MspI) geno types and allele frequencies in the Chinese. The frequency of the rarer allele (M2) in the Chinese was found to be higher than in Cauca sians (0.3 vs. 0.16, respectively; y} = 5.27, p <0.025) (23). The distribution of genotypes of this RFLP showed a close fit to the HardyWeinberg equilibrium in the Chinese.…”

Section: Resultsmentioning

confidence: 72%

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Mspl Polymorphism of the Apohpoprotein A-II Gene, Serum Lipids and Apolipoproteins in Chinese from Singapore

Saha

Tan²,

Tay³

1992

Hum Hered

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The effect of a DNA polymorphism (Mspl) of the apohpoprotein (apo) A-II gene on serum lipid and apo levels was studied in a group of 125 healthy Chinese of both sexes. The frequency of the 3.7-kb rarer allele (M2) was found to be significantly higher in the Chinese (0.30) than in Caucasians (0.16; p < 0.025). The distribution of apo A-II genotypes was in Hardy-Weinberg equilibrium in the Chinese population. The presence of a polymorphic site (Mspl) within an Alu sequence at the 3’ end of the gene, the 3.0 kb (M1)allele, was associated with significantly higher levels of serum apo A-I and A-II (p < 0.05 and < 0.01, respectively). Serum high-density Lipo-protein cholesterol levels were also correspondingly higher in individuals with M1, but did not reach a significant level. Male heterozygotes of the apo A-II polymorphism had significantly higher levels of serum triglycerides compared to homozygotes (p < 0.05). Thus the Mspl polymorphism of the apo A-II gene appears to be associated with altered levels of lipids and apos in the Chinese population.

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Genetics of cerebrovascular disease

Massa¹,

Sharp²

1999

Ann Neurol.

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Plasma lipoprotein lipids in relation to the MspI polymorphism of the apolipoprotein All gene in Caucasian men Lack of association with plasma triglyceride concentration

Cited by 18 publications

References 15 publications

Evidence for linkage of the apolipoprotein A-II locus to plasma apolipoprotein A-II and free fatty acid levels in mice and humans.

Evidence for linkage of the apolipoprotein A-II locus to plasma apolipoprotein A-II and free fatty acid levels in mice and humans.

Mspl Polymorphism of the Apohpoprotein A-II Gene, Serum Lipids and Apolipoproteins in Chinese from Singapore

Genetics of cerebrovascular disease

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