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Xiaomin Zhang - One of the best experts on this subject based on the ideXlab platform.
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interaction of polymorphisms in APOA4 apoa5 zpr1 bud13 gene cluster and sleep duration on 5 year lipid changes in middle aged and older chinese
Sleep, 2019Co-Authors: Liangle Yang, Wenting Guo, Qin Fang, Xuefeng Lai, Xiaomin ZhangAbstract:STUDY OBJECTIVES Lipid profiles are influenced by both genetic and environmental factors. Genetic variants in the APOA4-APOA5-ZPR1-BUD13 gene cluster and aberrant sleep duration were independently identified to be associated with lipids in previous studies. We aimed to investigate whether sleep duration modified the genetic associations with longitudinal lipids changes. METHODS Four single nucleotide polymorphisms (SNPs), rs17119975, rs651821, rs7396835, and rs964184 in the APOA4-APOA5-ZPR1-BUD13 gene cluster were genotyped among 8648 apparently healthy subjects from the Dongfeng-Tongji (DFTJ) cohort. Information on sleep duration was obtained by questionnaires. Changes in total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), were evaluated from baseline to 5-year follow-up. RESULTS After multivariate adjustments, we found that rs651821 and weighted genetic risk score (GRS) were significantly associated with increased triglyceride, and the genetic association with triglyceride change consistently strengthened across sleep duration categories. The differences in triglyceride changes per increment of risk allele for rs651821 were 0.028 (SE = 0.017, p = 0.112), 0.051 (SE = 0.009, p 7-<9, and ≥9 h, respectively (p interaction = 0.031). The GRS also showed a significant interaction with sleep duration categories for triglyceride change (p interaction = 0.010). In addition, all of the four SNPs and GRS were inversely related to HDL-c changes. CONCLUSIONS Longer sleep duration might exacerbate the adverse effects of SNPs in APOA4-APOA5-ZPR1-BUD13 gene cluster on 5-year triglyceride changes.
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Interaction of polymorphisms in APOA4-APOA5-ZPR1-BUD13 gene cluster and sleep duration on 5-year lipid changes in middle aged and older Chinese.
Sleep, 2019Co-Authors: Liangle Yang, Wenting Guo, Qin Fang, Xuefeng Lai, Xiaomin ZhangAbstract:STUDY OBJECTIVES Lipid profiles are influenced by both genetic and environmental factors. Genetic variants in the APOA4-APOA5-ZPR1-BUD13 gene cluster and aberrant sleep duration were independently identified to be associated with lipids in previous studies. We aimed to investigate whether sleep duration modified the genetic associations with longitudinal lipids changes. METHODS Four single nucleotide polymorphisms (SNPs), rs17119975, rs651821, rs7396835, and rs964184 in the APOA4-APOA5-ZPR1-BUD13 gene cluster were genotyped among 8648 apparently healthy subjects from the Dongfeng-Tongji (DFTJ) cohort. Information on sleep duration was obtained by questionnaires. Changes in total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), were evaluated from baseline to 5-year follow-up. RESULTS After multivariate adjustments, we found that rs651821 and weighted genetic risk score (GRS) were significantly associated with increased triglyceride, and the genetic association with triglyceride change consistently strengthened across sleep duration categories. The differences in triglyceride changes per increment of risk allele for rs651821 were 0.028 (SE = 0.017, p = 0.112), 0.051 (SE = 0.009, p 7-
Philippa J Talmud - One of the best experts on this subject based on the ideXlab platform.
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APOE, CETP and LPL genes show strong association with lipid levels in Greek children
Nutrition metabolism and cardiovascular diseases : NMCD, 2009Co-Authors: Melissa C. Smart, Steve E Humphries, George Dedoussis, Eirini Louizou, Mary Yannakoulia, F Drenos, Constantina Papoutsakis, Nikolas Maniatis, Philippa J TalmudAbstract:Abstract Background and aims Studies have consistently demonstrated that variants in a number of candidate genes are significant determinants of lipid levels in adults. However, few studies have investigated the impact of these variants in children. Therefore, in the present investigation we examined the influence of ten common variants in the genes for lipoprotein lipase ( LPL – S447X), cholesterol ester transfer protein ( CETP – Taq 1B) apolipoprotein ( APO ) E (ɛ2, ɛ3, ɛ4), APOA5 (−1131C>T and S19W), APOA4 (S347T) and APOC3 (−482C>T; 1100C>T and 3238G>C) on lipoprotein levels children from the Gene–Diet Attica Investigation on childhood obesity (GENDAI). Methods and results The ten variants selected were genotyped in 882 Greek children, mean age: 11.2±0.7 years (418 females and 464 males). Genotypes were assessed using Taq Man technology. Significantly higher total cholesterol (TC) ( p =0.0001) and low-density lipoprotein cholesterol (LDL-C) ( p APOE ɛ4 carriers compared to ɛ3/ɛ3 homozygotes and ɛ2 carriers. The association of APOE genotype with TC and high-density lipoprotein cholesterol (HDL-C) ratio ( p =0.0008) was further modulated by body mass index. Carriers of the CETP Taq IB B2 allele had significantly higher HDL-C ( p p APOA4 , APOA5 and APOC3 variants and serum lipids. Conclusion This study demonstrates that these common variants are associated with lipid levels in this healthy paediatric cohort, suggesting that even in these young children there may be potential in predicting their lifelong exposure to an adverse lipid profile.
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The APOA4 T347S variant is associated with reduced plasma TAOS in subjects with diabetes mellitus and cardiovascular disease.
Journal of lipid research, 2004Co-Authors: Wai-man R. Wong, Steve E Humphries, Jeffrey W. Stephens, Jayshree Acharya, Steven J. Hurel, Philippa J TalmudAbstract:Apolipoprotein A-IV (apoA-IV) has been postulated to be antiatherogenic. Transgenic APOA4/Apoe-/- mice are protected against atherosclerosis, with plasma apoA-IV displaying antioxidant activity in vitro. In humans, there is an inverse relationship between apoA-IV levels and risk of coronary heart disease (CHD). Furthermore, the APOA4 T347S rare allele has been associated with increased risk of CHD and reduced apoA-IV levels. Reduced total antioxidant status (TAOS) due to increased oxidative stress is implicated in the process of atherogenesis. Thus, this study aimed to examine the association between the APOA4 T347S variant and TAOS in diabetic patients with (n = 196) or without (n = 509) cardiovascular disease (CVD). A higher percentage of CVD patients were present in the lowest quartile of TAOS, compared with the rest (P = 0.04). Overall, there was no association between genotype and TAOS. However, in patients with CVD, homozygotes for the S347 allele had significantly lower TAOS compared with TT and TS subjects (31.2 +/- 9.89% and 42.5 +/- 13.04% TAOS, respectively; P = 0.0024), an effect that was not seen in the patients without CVD. This study offers direct support for an antioxidant capacity of apoA-IV, thus providing some explanation for the antiatherogenic role of apoA-IV and the higher CVD risk in S347 homozygotes.
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relative contribution of variation within the apoc3 a4 a5 gene cluster in determining plasma triglycerides
Human Molecular Genetics, 2002Co-Authors: Philippa J Talmud, Len A. Pennacchio, Edward M. Rubin, Emma Hawe, Steve Martin, Michael Olivier, George J Miller, Steve E HumphriesAbstract:Since triglycerides (TG) are a major independent risk factor for coronary heart disease, understanding their genetic and environmental determinants is of major importance. Mouse models indicate an inverse relationship between levels of the newly identified apolipoprotein AV (APOAV) and TG concentrations. We have examined the relative influence of human APOA5 variants on plasma lipids, compared to the impact of variation in APOC3 and APOA4 which lie in the same cluster. Single nucleotide polymorphisms (SNPs) in APOA5 (S19W, -1131T>C) and APOA4 (T347S, Q360H) and an APOA4/A5 intergenic T>C SNP were examined in a large study of healthy middle-aged men (n=2808). APOA5 19WW and -1131CC men had 52% and 40% higher TG (P G, -482C>T, 1100C>T, and 3238C>G). The major TG-raising alleles were defined by APOA5 W19 and APOC3 -482T. This suggests that the TG-lowering effect of APOA4 S347 might merely reflect the strong negative linkage disequilibrium with the common alleles of these variants. Thus variation in APOA5 is associated with differences in TGs in healthy men, independent of those previously reported for APOC3, while association between APOA4 and TG reflects linkage disequilibrium with these sites. The molecular mechanisms for these effects remain to be determined.
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Relative contribution of variation within the APOC3/A4/A5 gene cluster in determining plasma triglycerides
Human molecular genetics, 2002Co-Authors: Philippa J Talmud, Len A. Pennacchio, Edward M. Rubin, Emma Hawe, Steve Martin, Michael Olivier, George J Miller, Steve E HumphriesAbstract:Since triglycerides (TG) are a major independent risk factor for coronary heart disease, understanding their genetic and environmental determinants is of major importance. Mouse models indicate an inverse relationship between levels of the newly identified apolipoprotein AV (APOAV) and TG concentrations. We have examined the relative influence of human APOA5 variants on plasma lipids, compared to the impact of variation in APOC3 and APOA4 which lie in the same cluster. Single nucleotide polymorphisms (SNPs) in APOA5 (S19W, -1131T>C) and APOA4 (T347S, Q360H) and an APOA4/A5 intergenic T>C SNP were examined in a large study of healthy middle-aged men (n=2808). APOA5 19WW and -1131CC men had 52% and 40% higher TG (P G, -482C>T, 1100C>T, and 3238C>G). The major TG-raising alleles were defined by APOA5 W19 and APOC3 -482T. This suggests that the TG-lowering effect of APOA4 S347 might merely reflect the strong negative linkage disequilibrium with the common alleles of these variants. Thus variation in APOA5 is associated with differences in TGs in healthy men, independent of those previously reported for APOC3, while association between APOA4 and TG reflects linkage disequilibrium with these sites. The molecular mechanisms for these effects remain to be determined.
Li Zhou - One of the best experts on this subject based on the ideXlab platform.
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Effects of Polymorphisms in APOA4-APOA5-ZNF259-BUD13 Gene Cluster on Plasma Levels of Triglycerides and Risk of Coronary Heart Disease in a Chinese Han Population.
PloS one, 2015Co-Authors: Xiaojun Tang, Juan Chen, Mingjun Zhang, Long Wang, Jinjin Jing, Li ZhouAbstract:Background/Aim Recent genome-wide association studies have identified several loci influencing lipid levels. The present study focused on the triglycerides (TG)-associated locus, the APOA4-APOA5-ZNF259-BUD13 gene cluster on chromosome 11, to explore the role of genetic variants in this gene cluster in the development of increasing TG levels and coronary heart disease (CHD). Methodology/Principal Findings Six single nucleotide polymorphisms (SNPs), rs4417316, rs651821, rs6589566, rs7396835, rs964184 and rs17119975, in the APOA4-APOA5-ZNF259-BUD13 gene cluster were selected and genotyped in 5374 healthy Chinese subjects. There were strong significant associations between the six SNPs and TG levels (P
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effects of polymorphisms in APOA4 apoa5 znf259 bud13 gene cluster on plasma levels of triglycerides and risk of coronary heart disease in a chinese han population
PLOS ONE, 2015Co-Authors: Xiaojun Tang, Juan Chen, Mingjun Zhang, Long Wang, Jinjin Jing, Li ZhouAbstract:Background/Aim Recent genome-wide association studies have identified several loci influencing lipid levels. The present study focused on the triglycerides (TG)-associated locus, the APOA4-APOA5-ZNF259-BUD13 gene cluster on chromosome 11, to explore the role of genetic variants in this gene cluster in the development of increasing TG levels and coronary heart disease (CHD). Methodology/Principal Findings Six single nucleotide polymorphisms (SNPs), rs4417316, rs651821, rs6589566, rs7396835, rs964184 and rs17119975, in the APOA4-APOA5-ZNF259-BUD13 gene cluster were selected and genotyped in 5374 healthy Chinese subjects. There were strong significant associations between the six SNPs and TG levels (P<1.0×10−8). Moreover, a weighted genotype score was found to be associated with TG levels (P = 3.28×10−13). The frequencies of three common haplotypes were observed to be significantly different between the high TG group and the low TG group (P<0.05). However, no significant effects were found for the SNPs regarding susceptibility to CHD in the Chinese case-control populations. Conclusions/Significance This study highlights the genotypes, genotype scores and haplotypes of the APOA4-APOA5-ZNF259-BUD13 gene cluster that were associated with TG levels in a Chinese population; however, the genetic variants in this gene cluster did not increase the risk of CHD in the Chinese population.
Steve E Humphries - One of the best experts on this subject based on the ideXlab platform.
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APOE, CETP and LPL genes show strong association with lipid levels in Greek children
Nutrition metabolism and cardiovascular diseases : NMCD, 2009Co-Authors: Melissa C. Smart, Steve E Humphries, George Dedoussis, Eirini Louizou, Mary Yannakoulia, F Drenos, Constantina Papoutsakis, Nikolas Maniatis, Philippa J TalmudAbstract:Abstract Background and aims Studies have consistently demonstrated that variants in a number of candidate genes are significant determinants of lipid levels in adults. However, few studies have investigated the impact of these variants in children. Therefore, in the present investigation we examined the influence of ten common variants in the genes for lipoprotein lipase ( LPL – S447X), cholesterol ester transfer protein ( CETP – Taq 1B) apolipoprotein ( APO ) E (ɛ2, ɛ3, ɛ4), APOA5 (−1131C>T and S19W), APOA4 (S347T) and APOC3 (−482C>T; 1100C>T and 3238G>C) on lipoprotein levels children from the Gene–Diet Attica Investigation on childhood obesity (GENDAI). Methods and results The ten variants selected were genotyped in 882 Greek children, mean age: 11.2±0.7 years (418 females and 464 males). Genotypes were assessed using Taq Man technology. Significantly higher total cholesterol (TC) ( p =0.0001) and low-density lipoprotein cholesterol (LDL-C) ( p APOE ɛ4 carriers compared to ɛ3/ɛ3 homozygotes and ɛ2 carriers. The association of APOE genotype with TC and high-density lipoprotein cholesterol (HDL-C) ratio ( p =0.0008) was further modulated by body mass index. Carriers of the CETP Taq IB B2 allele had significantly higher HDL-C ( p p APOA4 , APOA5 and APOC3 variants and serum lipids. Conclusion This study demonstrates that these common variants are associated with lipid levels in this healthy paediatric cohort, suggesting that even in these young children there may be potential in predicting their lifelong exposure to an adverse lipid profile.
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The APOA4 T347S variant is associated with reduced plasma TAOS in subjects with diabetes mellitus and cardiovascular disease.
Journal of lipid research, 2004Co-Authors: Wai-man R. Wong, Steve E Humphries, Jeffrey W. Stephens, Jayshree Acharya, Steven J. Hurel, Philippa J TalmudAbstract:Apolipoprotein A-IV (apoA-IV) has been postulated to be antiatherogenic. Transgenic APOA4/Apoe-/- mice are protected against atherosclerosis, with plasma apoA-IV displaying antioxidant activity in vitro. In humans, there is an inverse relationship between apoA-IV levels and risk of coronary heart disease (CHD). Furthermore, the APOA4 T347S rare allele has been associated with increased risk of CHD and reduced apoA-IV levels. Reduced total antioxidant status (TAOS) due to increased oxidative stress is implicated in the process of atherogenesis. Thus, this study aimed to examine the association between the APOA4 T347S variant and TAOS in diabetic patients with (n = 196) or without (n = 509) cardiovascular disease (CVD). A higher percentage of CVD patients were present in the lowest quartile of TAOS, compared with the rest (P = 0.04). Overall, there was no association between genotype and TAOS. However, in patients with CVD, homozygotes for the S347 allele had significantly lower TAOS compared with TT and TS subjects (31.2 +/- 9.89% and 42.5 +/- 13.04% TAOS, respectively; P = 0.0024), an effect that was not seen in the patients without CVD. This study offers direct support for an antioxidant capacity of apoA-IV, thus providing some explanation for the antiatherogenic role of apoA-IV and the higher CVD risk in S347 homozygotes.
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relative contribution of variation within the apoc3 a4 a5 gene cluster in determining plasma triglycerides
Human Molecular Genetics, 2002Co-Authors: Philippa J Talmud, Len A. Pennacchio, Edward M. Rubin, Emma Hawe, Steve Martin, Michael Olivier, George J Miller, Steve E HumphriesAbstract:Since triglycerides (TG) are a major independent risk factor for coronary heart disease, understanding their genetic and environmental determinants is of major importance. Mouse models indicate an inverse relationship between levels of the newly identified apolipoprotein AV (APOAV) and TG concentrations. We have examined the relative influence of human APOA5 variants on plasma lipids, compared to the impact of variation in APOC3 and APOA4 which lie in the same cluster. Single nucleotide polymorphisms (SNPs) in APOA5 (S19W, -1131T>C) and APOA4 (T347S, Q360H) and an APOA4/A5 intergenic T>C SNP were examined in a large study of healthy middle-aged men (n=2808). APOA5 19WW and -1131CC men had 52% and 40% higher TG (P G, -482C>T, 1100C>T, and 3238C>G). The major TG-raising alleles were defined by APOA5 W19 and APOC3 -482T. This suggests that the TG-lowering effect of APOA4 S347 might merely reflect the strong negative linkage disequilibrium with the common alleles of these variants. Thus variation in APOA5 is associated with differences in TGs in healthy men, independent of those previously reported for APOC3, while association between APOA4 and TG reflects linkage disequilibrium with these sites. The molecular mechanisms for these effects remain to be determined.
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Relative contribution of variation within the APOC3/A4/A5 gene cluster in determining plasma triglycerides
Human molecular genetics, 2002Co-Authors: Philippa J Talmud, Len A. Pennacchio, Edward M. Rubin, Emma Hawe, Steve Martin, Michael Olivier, George J Miller, Steve E HumphriesAbstract:Since triglycerides (TG) are a major independent risk factor for coronary heart disease, understanding their genetic and environmental determinants is of major importance. Mouse models indicate an inverse relationship between levels of the newly identified apolipoprotein AV (APOAV) and TG concentrations. We have examined the relative influence of human APOA5 variants on plasma lipids, compared to the impact of variation in APOC3 and APOA4 which lie in the same cluster. Single nucleotide polymorphisms (SNPs) in APOA5 (S19W, -1131T>C) and APOA4 (T347S, Q360H) and an APOA4/A5 intergenic T>C SNP were examined in a large study of healthy middle-aged men (n=2808). APOA5 19WW and -1131CC men had 52% and 40% higher TG (P G, -482C>T, 1100C>T, and 3238C>G). The major TG-raising alleles were defined by APOA5 W19 and APOC3 -482T. This suggests that the TG-lowering effect of APOA4 S347 might merely reflect the strong negative linkage disequilibrium with the common alleles of these variants. Thus variation in APOA5 is associated with differences in TGs in healthy men, independent of those previously reported for APOC3, while association between APOA4 and TG reflects linkage disequilibrium with these sites. The molecular mechanisms for these effects remain to be determined.
Liangle Yang - One of the best experts on this subject based on the ideXlab platform.
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interaction of polymorphisms in APOA4 apoa5 zpr1 bud13 gene cluster and sleep duration on 5 year lipid changes in middle aged and older chinese
Sleep, 2019Co-Authors: Liangle Yang, Wenting Guo, Qin Fang, Xuefeng Lai, Xiaomin ZhangAbstract:STUDY OBJECTIVES Lipid profiles are influenced by both genetic and environmental factors. Genetic variants in the APOA4-APOA5-ZPR1-BUD13 gene cluster and aberrant sleep duration were independently identified to be associated with lipids in previous studies. We aimed to investigate whether sleep duration modified the genetic associations with longitudinal lipids changes. METHODS Four single nucleotide polymorphisms (SNPs), rs17119975, rs651821, rs7396835, and rs964184 in the APOA4-APOA5-ZPR1-BUD13 gene cluster were genotyped among 8648 apparently healthy subjects from the Dongfeng-Tongji (DFTJ) cohort. Information on sleep duration was obtained by questionnaires. Changes in total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), were evaluated from baseline to 5-year follow-up. RESULTS After multivariate adjustments, we found that rs651821 and weighted genetic risk score (GRS) were significantly associated with increased triglyceride, and the genetic association with triglyceride change consistently strengthened across sleep duration categories. The differences in triglyceride changes per increment of risk allele for rs651821 were 0.028 (SE = 0.017, p = 0.112), 0.051 (SE = 0.009, p 7-<9, and ≥9 h, respectively (p interaction = 0.031). The GRS also showed a significant interaction with sleep duration categories for triglyceride change (p interaction = 0.010). In addition, all of the four SNPs and GRS were inversely related to HDL-c changes. CONCLUSIONS Longer sleep duration might exacerbate the adverse effects of SNPs in APOA4-APOA5-ZPR1-BUD13 gene cluster on 5-year triglyceride changes.
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Interaction of polymorphisms in APOA4-APOA5-ZPR1-BUD13 gene cluster and sleep duration on 5-year lipid changes in middle aged and older Chinese.
Sleep, 2019Co-Authors: Liangle Yang, Wenting Guo, Qin Fang, Xuefeng Lai, Xiaomin ZhangAbstract:STUDY OBJECTIVES Lipid profiles are influenced by both genetic and environmental factors. Genetic variants in the APOA4-APOA5-ZPR1-BUD13 gene cluster and aberrant sleep duration were independently identified to be associated with lipids in previous studies. We aimed to investigate whether sleep duration modified the genetic associations with longitudinal lipids changes. METHODS Four single nucleotide polymorphisms (SNPs), rs17119975, rs651821, rs7396835, and rs964184 in the APOA4-APOA5-ZPR1-BUD13 gene cluster were genotyped among 8648 apparently healthy subjects from the Dongfeng-Tongji (DFTJ) cohort. Information on sleep duration was obtained by questionnaires. Changes in total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), were evaluated from baseline to 5-year follow-up. RESULTS After multivariate adjustments, we found that rs651821 and weighted genetic risk score (GRS) were significantly associated with increased triglyceride, and the genetic association with triglyceride change consistently strengthened across sleep duration categories. The differences in triglyceride changes per increment of risk allele for rs651821 were 0.028 (SE = 0.017, p = 0.112), 0.051 (SE = 0.009, p 7-