Genetic polymorphisms of the SHBG gene can be the effect on SHBG and HDL-cholesterol levels in Coronary Heart Disease: a case–control study

Sex hormone binding globulin (SHBG) level is positively associated with the high-density lipoprotein cholesterol (HDL-C) levels. The aim of this study was to investigate the effects of the SHBG gene variations (D356N, rs1799941, and P156L) on SHBG and HDL-C levels and Coronary Heart Disease (CHD) ri...

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Veröffentlicht in:Molecular biology reports 2019-08, Vol.46 (4), p.4259-4269
Hauptverfasser: Kurnaz-Gomleksiz, Ozlem, Akadam-Teker, Basak, Bugra, Zehra, Omer, Beyhan, Yilmaz-Aydogan, Hulya
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Akadam-Teker, Basak
Bugra, Zehra
Omer, Beyhan
Yilmaz-Aydogan, Hulya
description Sex hormone binding globulin (SHBG) level is positively associated with the high-density lipoprotein cholesterol (HDL-C) levels. The aim of this study was to investigate the effects of the SHBG gene variations (D356N, rs1799941, and P156L) on SHBG and HDL-C levels and Coronary Heart Disease (CHD) risk. The SHBG D356 N (rs6259,G > A), P156L (rs6258,C > T), and rs1799941(G > A) polymorphisms were determined in 131 male CHD patients and 55 male controls by PCR-RFLP and real-time PCR techniques. SHGB levels were measured by Electro-chemiluminescence immunoassay (ECLIA). In the patients who had SHBG levels lower than threshold 35 nmol/l value, the risk of being HDL-C levels lower than threshold 0.90 mmol/l value was observed statistically significant (p = 0.017; OR 2.522, 95% CI 1.170–5.438). The rs1799941 GG was associated with increased CHD risk when compared with the A allele carriers (GA + AA) (p = 0.019, OR 2.222, 95% CI 1.130–4.371). In addition, the rs1799941 GG genotype and D356 N N allele were associated with lower SHBG in the CHD group (p 
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The aim of this study was to investigate the effects of the SHBG gene variations (D356N, rs1799941, and P156L) on SHBG and HDL-C levels and Coronary Heart Disease (CHD) risk. The SHBG D356 N (rs6259,G &gt; A), P156L (rs6258,C &gt; T), and rs1799941(G &gt; A) polymorphisms were determined in 131 male CHD patients and 55 male controls by PCR-RFLP and real-time PCR techniques. SHGB levels were measured by Electro-chemiluminescence immunoassay (ECLIA). In the patients who had SHBG levels lower than threshold 35 nmol/l value, the risk of being HDL-C levels lower than threshold 0.90 mmol/l value was observed statistically significant (p = 0.017; OR 2.522, 95% CI 1.170–5.438). The rs1799941 GG was associated with increased CHD risk when compared with the A allele carriers (GA + AA) (p = 0.019, OR 2.222, 95% CI 1.130–4.371). In addition, the rs1799941 GG genotype and D356 N N allele were associated with lower SHBG in the CHD group (p &lt; 0.01). The logistic regression analysis also revealed the rs1799941 GG genotype was significantly associated with low SHBG in CHD patients. It was observed that Haplotype-1(rs1799941 G allele—P156L P allele—D356 N D allele) was associated with increased CHD risk, while Haplotype-2 (rs1799941 rare A allele-P156L C allele- D356 N G allele) was correlated with the decreased CHD risk (p = 0.0167). 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The aim of this study was to investigate the effects of the SHBG gene variations (D356N, rs1799941, and P156L) on SHBG and HDL-C levels and Coronary Heart Disease (CHD) risk. The SHBG D356 N (rs6259,G &gt; A), P156L (rs6258,C &gt; T), and rs1799941(G &gt; A) polymorphisms were determined in 131 male CHD patients and 55 male controls by PCR-RFLP and real-time PCR techniques. SHGB levels were measured by Electro-chemiluminescence immunoassay (ECLIA). In the patients who had SHBG levels lower than threshold 35 nmol/l value, the risk of being HDL-C levels lower than threshold 0.90 mmol/l value was observed statistically significant (p = 0.017; OR 2.522, 95% CI 1.170–5.438). The rs1799941 GG was associated with increased CHD risk when compared with the A allele carriers (GA + AA) (p = 0.019, OR 2.222, 95% CI 1.130–4.371). In addition, the rs1799941 GG genotype and D356 N N allele were associated with lower SHBG in the CHD group (p &lt; 0.01). The logistic regression analysis also revealed the rs1799941 GG genotype was significantly associated with low SHBG in CHD patients. It was observed that Haplotype-1(rs1799941 G allele—P156L P allele—D356 N D allele) was associated with increased CHD risk, while Haplotype-2 (rs1799941 rare A allele-P156L C allele- D356 N G allele) was correlated with the decreased CHD risk (p = 0.0167). Our findings suggest that there is a positive correlation between SHBG and HDL-C levels in CHD patients, and this association might be affected by SHBG gene variations.</description><subject>Adult</subject><subject>Alleles</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Chemiluminescence</subject><subject>Cholesterol</subject><subject>Cholesterol, HDL - genetics</subject><subject>Coronary artery disease</subject><subject>coronary disease</subject><subject>Coronary Disease - genetics</subject><subject>electrochemiluminescence</subject><subject>Gene Frequency</subject><subject>Genotype</subject><subject>Globulins</subject><subject>Haplotypes</subject><subject>Health risk assessment</subject><subject>Heart diseases</subject><subject>High density lipoprotein</subject><subject>high density lipoprotein cholesterol</subject><subject>Histology</subject><subject>Humans</subject><subject>immunoassays</subject><subject>Life Sciences</subject><subject>Male</subject><subject>males</subject><subject>Middle Aged</subject><subject>Morphology</subject><subject>Original Article</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism, Single Nucleotide</subject><subject>quantitative polymerase chain reaction</subject><subject>regression analysis</subject><subject>Restriction fragment length polymorphism</subject><subject>risk</subject><subject>Risk Factors</subject><subject>Sex Hormone-Binding Globulin - genetics</subject><subject>Sex Hormone-Binding Globulin - metabolism</subject><subject>Statistical analysis</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkcFu1DAQhi0EokvhBTggS1x6CYxjO064wRZ2K1XiAJwtxxl3UyX2Yieoe-sLcOINeRLcpgWJA_hiyfP9_4znJ-Q5g1cMQL1OjAHnBbCmAFHXUFw9ICsmFS9Eo-qHZAUcWCFqyY7Ik5QuAUAwJR-TI87y4VWzIt836HHqLd2H4TCGuN_1aUw0ODrtkH7avtvQi0xQazxt8fYRnUM70eCXsvEd3Z6eF3YXBkwTxjDQAb_hkGjv6TrE4E080C2aONHTPqFJ-Iaa7Jjw5_UPG_x0I0nT3B2ekkfODAmf3d3H5MuH95_X2-L84-Zs_TY3EVBPhRGAleCgmo67zlleOSltK1nXGC54y5xlDruqASmZUa52VphS2drxpq1aw4_JyeK7j-HrnKfWY58sDoPxGOakSw6SNZIL-D9a8hIyqnhGX_6FXoY5-vyRTJWqyguvRabKhbIxpBTR6X3sx7wizUDf5KqXXHXOVd_mqq-y6MWd9dyO2P2W3AeZAb4AKZf8BcY_vf9h-wvWkK69</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Kurnaz-Gomleksiz, Ozlem</creator><creator>Akadam-Teker, Basak</creator><creator>Bugra, Zehra</creator><creator>Omer, Beyhan</creator><creator>Yilmaz-Aydogan, Hulya</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-9904-0146</orcidid><orcidid>https://orcid.org/0000-0001-7938-6281</orcidid><orcidid>https://orcid.org/0000-0003-3618-0560</orcidid><orcidid>https://orcid.org/0000-0001-9827-5253</orcidid><orcidid>https://orcid.org/0000-0002-8837-6664</orcidid></search><sort><creationdate>20190801</creationdate><title>Genetic polymorphisms of the SHBG gene can be the effect on SHBG and HDL-cholesterol levels in Coronary Heart Disease: a case–control study</title><author>Kurnaz-Gomleksiz, Ozlem ; 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The aim of this study was to investigate the effects of the SHBG gene variations (D356N, rs1799941, and P156L) on SHBG and HDL-C levels and Coronary Heart Disease (CHD) risk. The SHBG D356 N (rs6259,G &gt; A), P156L (rs6258,C &gt; T), and rs1799941(G &gt; A) polymorphisms were determined in 131 male CHD patients and 55 male controls by PCR-RFLP and real-time PCR techniques. SHGB levels were measured by Electro-chemiluminescence immunoassay (ECLIA). In the patients who had SHBG levels lower than threshold 35 nmol/l value, the risk of being HDL-C levels lower than threshold 0.90 mmol/l value was observed statistically significant (p = 0.017; OR 2.522, 95% CI 1.170–5.438). The rs1799941 GG was associated with increased CHD risk when compared with the A allele carriers (GA + AA) (p = 0.019, OR 2.222, 95% CI 1.130–4.371). In addition, the rs1799941 GG genotype and D356 N N allele were associated with lower SHBG in the CHD group (p &lt; 0.01). The logistic regression analysis also revealed the rs1799941 GG genotype was significantly associated with low SHBG in CHD patients. It was observed that Haplotype-1(rs1799941 G allele—P156L P allele—D356 N D allele) was associated with increased CHD risk, while Haplotype-2 (rs1799941 rare A allele-P156L C allele- D356 N G allele) was correlated with the decreased CHD risk (p = 0.0167). Our findings suggest that there is a positive correlation between SHBG and HDL-C levels in CHD patients, and this association might be affected by SHBG gene variations.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>31111369</pmid><doi>10.1007/s11033-019-04880-x</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-9904-0146</orcidid><orcidid>https://orcid.org/0000-0001-7938-6281</orcidid><orcidid>https://orcid.org/0000-0003-3618-0560</orcidid><orcidid>https://orcid.org/0000-0001-9827-5253</orcidid><orcidid>https://orcid.org/0000-0002-8837-6664</orcidid></addata></record>
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source MEDLINE; Springer Nature - Complete Springer Journals
subjects Adult
Alleles
Animal Anatomy
Animal Biochemistry
Biomedical and Life Sciences
Cardiovascular disease
Case-Control Studies
Chemiluminescence
Cholesterol
Cholesterol, HDL - genetics
Coronary artery disease
coronary disease
Coronary Disease - genetics
electrochemiluminescence
Gene Frequency
Genotype
Globulins
Haplotypes
Health risk assessment
Heart diseases
High density lipoprotein
high density lipoprotein cholesterol
Histology
Humans
immunoassays
Life Sciences
Male
males
Middle Aged
Morphology
Original Article
Polymerase chain reaction
Polymorphism, Single Nucleotide
quantitative polymerase chain reaction
regression analysis
Restriction fragment length polymorphism
risk
Risk Factors
Sex Hormone-Binding Globulin - genetics
Sex Hormone-Binding Globulin - metabolism
Statistical analysis
title Genetic polymorphisms of the SHBG gene can be the effect on SHBG and HDL-cholesterol levels in Coronary Heart Disease: a case–control study
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