Linkage and linkage disequilibrium analysis of the lipoprotein lipase gene with lipid profiles in Chinese hypertensive families

Wenjie Yang, Jianfeng Huang, Cailiang Yao, Shaoyong Su, Donghai Liu, Dongliang Ge, Dongfeng Gu

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Elevated TG [triacylglycerol (triglyceide)] is a significant independent risk factor for cardiovascular disease. LPL (lipoprotein lipase) is one of the key enzymes in the metabolism of the TG-rich lipoproteins which hydrolyses TG from the chylomicrons and very-LDL (low-density lipoprotein). To investigate the relationship between the LPL gene and lipid profiles, especially TG, in 148 hypertensive families, we have chosen seven flanking microsatellite markers and four internal markers of the LPL gene and conducted linkage analysis by SOLAR and S.A.G.E. (statistical analysis for genetic epidemiology)/SIBPAL 2 programs, and linkage disequilibrium analysis by QTDT (quantitative transmission/ disequilibrium test) and GOLD (graphical overview of linkage disequilibrium). There were statistically significant differences in lipid levels between subjects without and with hypertension within families. A maximum LOD score of 1.3 with TG at the marker D8S261 was observed by SOLAR. Using S.A.G.E./SIBPAL 2, we identified a linkage with TG at the marker 'ATTT' located within intron 6 of the LPL gene (P = 0.0095). Two SNPs (single nucleotide polymorphisms), HindIII and HinfI, were found in linkage disequilibrium with LDL-cholesterol levels (P = 0.0178 and P = 0.0088 respectively). A strong linkage disequilibrium was observed between the HindIII in intron 8 and HinfI in the exon 9 (P < 0.00001, D′ = 0.895). Linkage disequilibrium was also found between the 'ATTT' polymorphism in intron 6 and two SNPs (P = 0.0021 and D′ = 0.611 for HindIII; and P = 0.00004, D′ = 0.459 for HinfI). The present study in the Chinese families with hypertension suggested that the LPL gene might influence lipid levels, especially TG metabolism. Replication studies both in Chinese and other populations are warranted to confirm these results.

Original languageEnglish (US)
Pages (from-to)137-142
Number of pages6
JournalClinical Science
Volume108
Issue number2
DOIs
StatePublished - Feb 1 2005

Fingerprint

Lipoprotein Lipase
Linkage Disequilibrium
Triglycerides
Lipids
Genes
Introns
Molecular Epidemiology
Single Nucleotide Polymorphism
Hypertension
Chylomicrons
VLDL Lipoproteins
Microsatellite Repeats
LDL Cholesterol
Lipoproteins
Exons
Cardiovascular Diseases
Enzymes
Population

Keywords

  • Hypertension
  • Linkage disequilibrium
  • Lipid
  • Lipoprotein lipase gene
  • Single nucleotide polymorphism
  • Triacylglycerol

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Linkage and linkage disequilibrium analysis of the lipoprotein lipase gene with lipid profiles in Chinese hypertensive families. / Yang, Wenjie; Huang, Jianfeng; Yao, Cailiang; Su, Shaoyong; Liu, Donghai; Ge, Dongliang; Gu, Dongfeng.

In: Clinical Science, Vol. 108, No. 2, 01.02.2005, p. 137-142.

Research output: Contribution to journalArticle

Yang, Wenjie ; Huang, Jianfeng ; Yao, Cailiang ; Su, Shaoyong ; Liu, Donghai ; Ge, Dongliang ; Gu, Dongfeng. / Linkage and linkage disequilibrium analysis of the lipoprotein lipase gene with lipid profiles in Chinese hypertensive families. In: Clinical Science. 2005 ; Vol. 108, No. 2. pp. 137-142.
@article{61d15dfe942d4e54be8d187e64195814,
title = "Linkage and linkage disequilibrium analysis of the lipoprotein lipase gene with lipid profiles in Chinese hypertensive families",
abstract = "Elevated TG [triacylglycerol (triglyceide)] is a significant independent risk factor for cardiovascular disease. LPL (lipoprotein lipase) is one of the key enzymes in the metabolism of the TG-rich lipoproteins which hydrolyses TG from the chylomicrons and very-LDL (low-density lipoprotein). To investigate the relationship between the LPL gene and lipid profiles, especially TG, in 148 hypertensive families, we have chosen seven flanking microsatellite markers and four internal markers of the LPL gene and conducted linkage analysis by SOLAR and S.A.G.E. (statistical analysis for genetic epidemiology)/SIBPAL 2 programs, and linkage disequilibrium analysis by QTDT (quantitative transmission/ disequilibrium test) and GOLD (graphical overview of linkage disequilibrium). There were statistically significant differences in lipid levels between subjects without and with hypertension within families. A maximum LOD score of 1.3 with TG at the marker D8S261 was observed by SOLAR. Using S.A.G.E./SIBPAL 2, we identified a linkage with TG at the marker 'ATTT' located within intron 6 of the LPL gene (P = 0.0095). Two SNPs (single nucleotide polymorphisms), HindIII and HinfI, were found in linkage disequilibrium with LDL-cholesterol levels (P = 0.0178 and P = 0.0088 respectively). A strong linkage disequilibrium was observed between the HindIII in intron 8 and HinfI in the exon 9 (P < 0.00001, D′ = 0.895). Linkage disequilibrium was also found between the 'ATTT' polymorphism in intron 6 and two SNPs (P = 0.0021 and D′ = 0.611 for HindIII; and P = 0.00004, D′ = 0.459 for HinfI). The present study in the Chinese families with hypertension suggested that the LPL gene might influence lipid levels, especially TG metabolism. Replication studies both in Chinese and other populations are warranted to confirm these results.",
keywords = "Hypertension, Linkage disequilibrium, Lipid, Lipoprotein lipase gene, Single nucleotide polymorphism, Triacylglycerol",
author = "Wenjie Yang and Jianfeng Huang and Cailiang Yao and Shaoyong Su and Donghai Liu and Dongliang Ge and Dongfeng Gu",
year = "2005",
month = "2",
day = "1",
doi = "10.1042/CS20040101",
language = "English (US)",
volume = "108",
pages = "137--142",
journal = "Clinical Science",
issn = "0143-5221",
publisher = "Portland Press Ltd.",
number = "2",

}

TY - JOUR

T1 - Linkage and linkage disequilibrium analysis of the lipoprotein lipase gene with lipid profiles in Chinese hypertensive families

AU - Yang, Wenjie

AU - Huang, Jianfeng

AU - Yao, Cailiang

AU - Su, Shaoyong

AU - Liu, Donghai

AU - Ge, Dongliang

AU - Gu, Dongfeng

PY - 2005/2/1

Y1 - 2005/2/1

N2 - Elevated TG [triacylglycerol (triglyceide)] is a significant independent risk factor for cardiovascular disease. LPL (lipoprotein lipase) is one of the key enzymes in the metabolism of the TG-rich lipoproteins which hydrolyses TG from the chylomicrons and very-LDL (low-density lipoprotein). To investigate the relationship between the LPL gene and lipid profiles, especially TG, in 148 hypertensive families, we have chosen seven flanking microsatellite markers and four internal markers of the LPL gene and conducted linkage analysis by SOLAR and S.A.G.E. (statistical analysis for genetic epidemiology)/SIBPAL 2 programs, and linkage disequilibrium analysis by QTDT (quantitative transmission/ disequilibrium test) and GOLD (graphical overview of linkage disequilibrium). There were statistically significant differences in lipid levels between subjects without and with hypertension within families. A maximum LOD score of 1.3 with TG at the marker D8S261 was observed by SOLAR. Using S.A.G.E./SIBPAL 2, we identified a linkage with TG at the marker 'ATTT' located within intron 6 of the LPL gene (P = 0.0095). Two SNPs (single nucleotide polymorphisms), HindIII and HinfI, were found in linkage disequilibrium with LDL-cholesterol levels (P = 0.0178 and P = 0.0088 respectively). A strong linkage disequilibrium was observed between the HindIII in intron 8 and HinfI in the exon 9 (P < 0.00001, D′ = 0.895). Linkage disequilibrium was also found between the 'ATTT' polymorphism in intron 6 and two SNPs (P = 0.0021 and D′ = 0.611 for HindIII; and P = 0.00004, D′ = 0.459 for HinfI). The present study in the Chinese families with hypertension suggested that the LPL gene might influence lipid levels, especially TG metabolism. Replication studies both in Chinese and other populations are warranted to confirm these results.

AB - Elevated TG [triacylglycerol (triglyceide)] is a significant independent risk factor for cardiovascular disease. LPL (lipoprotein lipase) is one of the key enzymes in the metabolism of the TG-rich lipoproteins which hydrolyses TG from the chylomicrons and very-LDL (low-density lipoprotein). To investigate the relationship between the LPL gene and lipid profiles, especially TG, in 148 hypertensive families, we have chosen seven flanking microsatellite markers and four internal markers of the LPL gene and conducted linkage analysis by SOLAR and S.A.G.E. (statistical analysis for genetic epidemiology)/SIBPAL 2 programs, and linkage disequilibrium analysis by QTDT (quantitative transmission/ disequilibrium test) and GOLD (graphical overview of linkage disequilibrium). There were statistically significant differences in lipid levels between subjects without and with hypertension within families. A maximum LOD score of 1.3 with TG at the marker D8S261 was observed by SOLAR. Using S.A.G.E./SIBPAL 2, we identified a linkage with TG at the marker 'ATTT' located within intron 6 of the LPL gene (P = 0.0095). Two SNPs (single nucleotide polymorphisms), HindIII and HinfI, were found in linkage disequilibrium with LDL-cholesterol levels (P = 0.0178 and P = 0.0088 respectively). A strong linkage disequilibrium was observed between the HindIII in intron 8 and HinfI in the exon 9 (P < 0.00001, D′ = 0.895). Linkage disequilibrium was also found between the 'ATTT' polymorphism in intron 6 and two SNPs (P = 0.0021 and D′ = 0.611 for HindIII; and P = 0.00004, D′ = 0.459 for HinfI). The present study in the Chinese families with hypertension suggested that the LPL gene might influence lipid levels, especially TG metabolism. Replication studies both in Chinese and other populations are warranted to confirm these results.

KW - Hypertension

KW - Linkage disequilibrium

KW - Lipid

KW - Lipoprotein lipase gene

KW - Single nucleotide polymorphism

KW - Triacylglycerol

UR - http://www.scopus.com/inward/record.url?scp=12944260588&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=12944260588&partnerID=8YFLogxK

U2 - 10.1042/CS20040101

DO - 10.1042/CS20040101

M3 - Article

C2 - 15482260

AN - SCOPUS:12944260588

VL - 108

SP - 137

EP - 142

JO - Clinical Science

JF - Clinical Science

SN - 0143-5221

IS - 2

ER -