author_facet Zhou, Xindie
Li, Jin
Jiang, Lifeng
Zhou, Dong
Wu, Lidong
Huang, Yong
Xu, Nanwei
Zhou, Xindie
Li, Jin
Jiang, Lifeng
Zhou, Dong
Wu, Lidong
Huang, Yong
Xu, Nanwei
author Zhou, Xindie
Li, Jin
Jiang, Lifeng
Zhou, Dong
Wu, Lidong
Huang, Yong
Xu, Nanwei
spellingShingle Zhou, Xindie
Li, Jin
Jiang, Lifeng
Zhou, Dong
Wu, Lidong
Huang, Yong
Xu, Nanwei
Bioscience Reports
SAA1 gene polymorphisms in osteoporosis patients
Cell Biology
Molecular Biology
Biochemistry
Biophysics
author_sort zhou, xindie
spelling Zhou, Xindie Li, Jin Jiang, Lifeng Zhou, Dong Wu, Lidong Huang, Yong Xu, Nanwei 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20181031 <jats:title>Abstract</jats:title> <jats:p>Background: Serum amyloid A (SAA1) is an apolipoprotein that maintains glucose and lipid homeostasis. Its polymorphisms are associated with risks of myocardial infarction and coronary artery disease (CAD). Methods: However, little is known about the associations of these polymorphisms with susceptibility to osteoporosis, which we evaluated in this hospital-based case–control study involving 300 osteoporosis patients and 350 controls. Three single-nucleotide polymorphisms (SNPs) (rs183978373, rs12218, and rs10832915) were genotyped using MALDI TOF MS. Results: There were no differences in the rs183978373 and rs12218 polymorphisms between the osteoporosis group and controls. The SAA1 gene rs10832915 polymorphism increased the risk of osteoporosis in our Chinese population. The genotypes of the rs10832915 polymorphism were not significantly associated with clinical parameters (age, body mass index (BMI), high- and low-density lipoprotein (LDL), total cholesterol (TC), and T-score). Haplotype analysis revealed that the ATT haplotype had a significant correlation with a decreased risk of osteoporosis. Conclusion: In conclusion, the SAA1 rs10832915 polymorphism and its haplotypes are associated with osteoporosis, but this finding should be confirmed in large well-designed studies.</jats:p> <i>SAA1</i> gene polymorphisms in osteoporosis patients Bioscience Reports
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title SAA1 gene polymorphisms in osteoporosis patients
title_unstemmed SAA1 gene polymorphisms in osteoporosis patients
title_full SAA1 gene polymorphisms in osteoporosis patients
title_fullStr SAA1 gene polymorphisms in osteoporosis patients
title_full_unstemmed SAA1 gene polymorphisms in osteoporosis patients
title_short SAA1 gene polymorphisms in osteoporosis patients
title_sort <i>saa1</i> gene polymorphisms in osteoporosis patients
topic Cell Biology
Molecular Biology
Biochemistry
Biophysics
url http://dx.doi.org/10.1042/bsr20181031
publishDate 2019
physical
description <jats:title>Abstract</jats:title> <jats:p>Background: Serum amyloid A (SAA1) is an apolipoprotein that maintains glucose and lipid homeostasis. Its polymorphisms are associated with risks of myocardial infarction and coronary artery disease (CAD). Methods: However, little is known about the associations of these polymorphisms with susceptibility to osteoporosis, which we evaluated in this hospital-based case–control study involving 300 osteoporosis patients and 350 controls. Three single-nucleotide polymorphisms (SNPs) (rs183978373, rs12218, and rs10832915) were genotyped using MALDI TOF MS. Results: There were no differences in the rs183978373 and rs12218 polymorphisms between the osteoporosis group and controls. The SAA1 gene rs10832915 polymorphism increased the risk of osteoporosis in our Chinese population. The genotypes of the rs10832915 polymorphism were not significantly associated with clinical parameters (age, body mass index (BMI), high- and low-density lipoprotein (LDL), total cholesterol (TC), and T-score). Haplotype analysis revealed that the ATT haplotype had a significant correlation with a decreased risk of osteoporosis. Conclusion: In conclusion, the SAA1 rs10832915 polymorphism and its haplotypes are associated with osteoporosis, but this finding should be confirmed in large well-designed studies.</jats:p>
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author Zhou, Xindie, Li, Jin, Jiang, Lifeng, Zhou, Dong, Wu, Lidong, Huang, Yong, Xu, Nanwei
author_facet Zhou, Xindie, Li, Jin, Jiang, Lifeng, Zhou, Dong, Wu, Lidong, Huang, Yong, Xu, Nanwei, Zhou, Xindie, Li, Jin, Jiang, Lifeng, Zhou, Dong, Wu, Lidong, Huang, Yong, Xu, Nanwei
author_sort zhou, xindie
container_issue 2
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container_title Bioscience Reports
container_volume 39
description <jats:title>Abstract</jats:title> <jats:p>Background: Serum amyloid A (SAA1) is an apolipoprotein that maintains glucose and lipid homeostasis. Its polymorphisms are associated with risks of myocardial infarction and coronary artery disease (CAD). Methods: However, little is known about the associations of these polymorphisms with susceptibility to osteoporosis, which we evaluated in this hospital-based case–control study involving 300 osteoporosis patients and 350 controls. Three single-nucleotide polymorphisms (SNPs) (rs183978373, rs12218, and rs10832915) were genotyped using MALDI TOF MS. Results: There were no differences in the rs183978373 and rs12218 polymorphisms between the osteoporosis group and controls. The SAA1 gene rs10832915 polymorphism increased the risk of osteoporosis in our Chinese population. The genotypes of the rs10832915 polymorphism were not significantly associated with clinical parameters (age, body mass index (BMI), high- and low-density lipoprotein (LDL), total cholesterol (TC), and T-score). Haplotype analysis revealed that the ATT haplotype had a significant correlation with a decreased risk of osteoporosis. Conclusion: In conclusion, the SAA1 rs10832915 polymorphism and its haplotypes are associated with osteoporosis, but this finding should be confirmed in large well-designed studies.</jats:p>
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spelling Zhou, Xindie Li, Jin Jiang, Lifeng Zhou, Dong Wu, Lidong Huang, Yong Xu, Nanwei 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20181031 <jats:title>Abstract</jats:title> <jats:p>Background: Serum amyloid A (SAA1) is an apolipoprotein that maintains glucose and lipid homeostasis. Its polymorphisms are associated with risks of myocardial infarction and coronary artery disease (CAD). Methods: However, little is known about the associations of these polymorphisms with susceptibility to osteoporosis, which we evaluated in this hospital-based case–control study involving 300 osteoporosis patients and 350 controls. Three single-nucleotide polymorphisms (SNPs) (rs183978373, rs12218, and rs10832915) were genotyped using MALDI TOF MS. Results: There were no differences in the rs183978373 and rs12218 polymorphisms between the osteoporosis group and controls. The SAA1 gene rs10832915 polymorphism increased the risk of osteoporosis in our Chinese population. The genotypes of the rs10832915 polymorphism were not significantly associated with clinical parameters (age, body mass index (BMI), high- and low-density lipoprotein (LDL), total cholesterol (TC), and T-score). Haplotype analysis revealed that the ATT haplotype had a significant correlation with a decreased risk of osteoporosis. Conclusion: In conclusion, the SAA1 rs10832915 polymorphism and its haplotypes are associated with osteoporosis, but this finding should be confirmed in large well-designed studies.</jats:p> <i>SAA1</i> gene polymorphisms in osteoporosis patients Bioscience Reports
spellingShingle Zhou, Xindie, Li, Jin, Jiang, Lifeng, Zhou, Dong, Wu, Lidong, Huang, Yong, Xu, Nanwei, Bioscience Reports, SAA1 gene polymorphisms in osteoporosis patients, Cell Biology, Molecular Biology, Biochemistry, Biophysics
title SAA1 gene polymorphisms in osteoporosis patients
title_full SAA1 gene polymorphisms in osteoporosis patients
title_fullStr SAA1 gene polymorphisms in osteoporosis patients
title_full_unstemmed SAA1 gene polymorphisms in osteoporosis patients
title_short SAA1 gene polymorphisms in osteoporosis patients
title_sort <i>saa1</i> gene polymorphisms in osteoporosis patients
title_unstemmed SAA1 gene polymorphisms in osteoporosis patients
topic Cell Biology, Molecular Biology, Biochemistry, Biophysics
url http://dx.doi.org/10.1042/bsr20181031