Leptin receptor Arg109 homozygotes display decreased total mortality as well as lower incidence of cardiovascular disease and related death.
Identifieur interne : 000201 ( PubMed/Curation ); précédent : 000200; suivant : 000202Leptin receptor Arg109 homozygotes display decreased total mortality as well as lower incidence of cardiovascular disease and related death.
Auteurs : Meiju Aij L [Finlande] ; Merja Santaniemi ; Risto Bloigu ; Y Antero Kes Niemi ; Olavi UkkolaSource :
- Gene ; 2014.
English descriptors
- KwdEn :
- Adult, Arginine (genetics), Cardiovascular Diseases (epidemiology), Cardiovascular Diseases (genetics), Cardiovascular Diseases (mortality), Coronary Disease (epidemiology), Coronary Disease (genetics), Female, Genotype, Homozygote, Humans, Incidence, Male, Middle Aged, Receptors, Leptin (genetics), Risk Factors.
- MESH :
- chemical , genetics : Arginine, Receptors, Leptin.
- epidemiology : Cardiovascular Diseases, Coronary Disease.
- genetics : Cardiovascular Diseases, Coronary Disease.
- mortality : Cardiovascular Diseases.
- Adult, Female, Genotype, Homozygote, Humans, Incidence, Male, Middle Aged, Risk Factors.
Abstract
Two leptin receptor single nucleotide polymorphisms, Lys109Arg and Gln223Arg, have been shown to associate with several risk factors for cardiovascular disease. In addition, we have previously shown that Arg109 and Arg223 homozygotes displayed lower intima-media thickness in our well-defined OPERA (Oulu Project Elucidating Risk of Atherosclerosis) study. This current research investigated the impact of these LEPR polymorphisms on cardiovascular events and related death as well as to total mortality in the 19-year follow-up of OPERA. Subjects were randomly selected, middle-aged drug-treated hypertensives and their age- and sex-matched control subjects recruited to the OPERA study between 1990 and 1993. Mortality and hospital events of 1045 subjects were followed up until 2009. A total of 151 coronary heart disease (CHD) and 211 cardiovascular disease (CVD) events or deaths including 58 CHD and 69 CVD deaths occurred. Furthermore, during this follow-up, a total of 165 subjects died. Logistic regression analysis was performed to assess the impact of Lys109Arg and Gln223Arg on the events and death. Further modeling was performed with Cox regression for Lys109Arg. The logistic regression analysis revealed a significant protective impact of Arg109Arg genotype on CHD (OR 0.433; CI 95% 0.217-0.863) and CVD (OR 0.540; CI 95% 0.309-0.942) events or death as well as on total mortality (OR 0.390; CI 95% 0.196-0.775) when adjusted with age, sex and study group. Even after further adjustment with BMI, smoking status, systolic blood pressure and low-density lipoprotein cholesterol, the protective effect of Arg109Arg on CHD events or death and total mortality still remained statistically significant (OR 0.463; CI 95% 0.230-0.931 and OR 0.442; CI 95% 0.218-0.896, respectively). Arg109Arg was also shown to confer protection against CHD mortality (HR 0.224; CI95% 0.055-0.919) and overall mortality (HR 0.413; CI95% 0.218-0.783) also in Cox regression analysis. In conclusion, the Arg109Arg genotype of LEPR seems to be protective from cardiovascular events and death and this phenomenon seems to be independent of the traditional risk factors for atherosclerosis.
DOI: 10.1016/j.gene.2013.10.003
PubMed: 24140454
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Leptin receptor Arg109 homozygotes display decreased total mortality as well as lower incidence of cardiovascular disease and related death.</title><author><name sortKey="Aij L, Meiju" sort="Aij L, Meiju" uniqKey="Aij L M" first="Meiju" last="Aij L">Meiju Aij L</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Clinical Medicine, Department of Internal Medicine and Biocenter Oulu, University of Oulu and Clinical Research Center, Oulu University Hospital, Oulu, Finland. Electronic address: meiju.aijala@oulu.fi.</nlm:affiliation><country xml:lang="fr">Finlande</country><wicri:regionArea>Institute of Clinical Medicine, Department of Internal Medicine and Biocenter Oulu, University of Oulu and Clinical Research Center, Oulu University Hospital, Oulu</wicri:regionArea></affiliation></author><author><name sortKey="Santaniemi, Merja" sort="Santaniemi, Merja" uniqKey="Santaniemi M" first="Merja" last="Santaniemi">Merja Santaniemi</name></author><author><name sortKey="Bloigu, Risto" sort="Bloigu, Risto" uniqKey="Bloigu R" first="Risto" last="Bloigu">Risto Bloigu</name></author><author><name sortKey="Kes Niemi, Y Antero" sort="Kes Niemi, Y Antero" uniqKey="Kes Niemi Y" first="Y Antero" last="Kes Niemi">Y Antero Kes Niemi</name></author><author><name sortKey="Ukkola, Olavi" sort="Ukkola, Olavi" uniqKey="Ukkola O" first="Olavi" last="Ukkola">Olavi Ukkola</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24140454</idno><idno type="pmid">24140454</idno><idno type="doi">10.1016/j.gene.2013.10.003</idno><idno type="wicri:Area/PubMed/Corpus">000201</idno><idno type="wicri:Area/PubMed/Curation">000201</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Leptin receptor Arg109 homozygotes display decreased total mortality as well as lower incidence of cardiovascular disease and related death.</title><author><name sortKey="Aij L, Meiju" sort="Aij L, Meiju" uniqKey="Aij L M" first="Meiju" last="Aij L">Meiju Aij L</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Clinical Medicine, Department of Internal Medicine and Biocenter Oulu, University of Oulu and Clinical Research Center, Oulu University Hospital, Oulu, Finland. Electronic address: meiju.aijala@oulu.fi.</nlm:affiliation><country xml:lang="fr">Finlande</country><wicri:regionArea>Institute of Clinical Medicine, Department of Internal Medicine and Biocenter Oulu, University of Oulu and Clinical Research Center, Oulu University Hospital, Oulu</wicri:regionArea></affiliation></author><author><name sortKey="Santaniemi, Merja" sort="Santaniemi, Merja" uniqKey="Santaniemi M" first="Merja" last="Santaniemi">Merja Santaniemi</name></author><author><name sortKey="Bloigu, Risto" sort="Bloigu, Risto" uniqKey="Bloigu R" first="Risto" last="Bloigu">Risto Bloigu</name></author><author><name sortKey="Kes Niemi, Y Antero" sort="Kes Niemi, Y Antero" uniqKey="Kes Niemi Y" first="Y Antero" last="Kes Niemi">Y Antero Kes Niemi</name></author><author><name sortKey="Ukkola, Olavi" sort="Ukkola, Olavi" uniqKey="Ukkola O" first="Olavi" last="Ukkola">Olavi Ukkola</name></author></analytic><series><title level="j">Gene</title><idno type="e-ISSN">1879-0038</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Arginine (genetics)</term><term>Cardiovascular Diseases (epidemiology)</term><term>Cardiovascular Diseases (genetics)</term><term>Cardiovascular Diseases (mortality)</term><term>Coronary Disease (epidemiology)</term><term>Coronary Disease (genetics)</term><term>Female</term><term>Genotype</term><term>Homozygote</term><term>Humans</term><term>Incidence</term><term>Male</term><term>Middle Aged</term><term>Receptors, Leptin (genetics)</term><term>Risk Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Arginine</term><term>Receptors, Leptin</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Cardiovascular Diseases</term><term>Coronary Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cardiovascular Diseases</term><term>Coronary Disease</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Cardiovascular Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Genotype</term><term>Homozygote</term><term>Humans</term><term>Incidence</term><term>Male</term><term>Middle Aged</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Two leptin receptor single nucleotide polymorphisms, Lys109Arg and Gln223Arg, have been shown to associate with several risk factors for cardiovascular disease. In addition, we have previously shown that Arg109 and Arg223 homozygotes displayed lower intima-media thickness in our well-defined OPERA (Oulu Project Elucidating Risk of Atherosclerosis) study. This current research investigated the impact of these LEPR polymorphisms on cardiovascular events and related death as well as to total mortality in the 19-year follow-up of OPERA. Subjects were randomly selected, middle-aged drug-treated hypertensives and their age- and sex-matched control subjects recruited to the OPERA study between 1990 and 1993. Mortality and hospital events of 1045 subjects were followed up until 2009. A total of 151 coronary heart disease (CHD) and 211 cardiovascular disease (CVD) events or deaths including 58 CHD and 69 CVD deaths occurred. Furthermore, during this follow-up, a total of 165 subjects died. Logistic regression analysis was performed to assess the impact of Lys109Arg and Gln223Arg on the events and death. Further modeling was performed with Cox regression for Lys109Arg. The logistic regression analysis revealed a significant protective impact of Arg109Arg genotype on CHD (OR 0.433; CI 95% 0.217-0.863) and CVD (OR 0.540; CI 95% 0.309-0.942) events or death as well as on total mortality (OR 0.390; CI 95% 0.196-0.775) when adjusted with age, sex and study group. Even after further adjustment with BMI, smoking status, systolic blood pressure and low-density lipoprotein cholesterol, the protective effect of Arg109Arg on CHD events or death and total mortality still remained statistically significant (OR 0.463; CI 95% 0.230-0.931 and OR 0.442; CI 95% 0.218-0.896, respectively). Arg109Arg was also shown to confer protection against CHD mortality (HR 0.224; CI95% 0.055-0.919) and overall mortality (HR 0.413; CI95% 0.218-0.783) also in Cox regression analysis. In conclusion, the Arg109Arg genotype of LEPR seems to be protective from cardiovascular events and death and this phenomenon seems to be independent of the traditional risk factors for atherosclerosis.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">24140454</PMID><DateCreated><Year>2013</Year><Month>11</Month><Day>25</Day></DateCreated><DateCompleted><Year>2014</Year><Month>01</Month><Day>17</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0038</ISSN><JournalIssue CitedMedium="Internet"><Volume>534</Volume><Issue>1</Issue><PubDate><Year>2014</Year><Month>Jan</Month><Day>15</Day></PubDate></JournalIssue><Title>Gene</Title><ISOAbbreviation>Gene</ISOAbbreviation></Journal><ArticleTitle>Leptin receptor Arg109 homozygotes display decreased total mortality as well as lower incidence of cardiovascular disease and related death.</ArticleTitle><Pagination><MedlinePgn>88-92</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.gene.2013.10.003</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0378-1119(13)01359-0</ELocationID><Abstract><AbstractText>Two leptin receptor single nucleotide polymorphisms, Lys109Arg and Gln223Arg, have been shown to associate with several risk factors for cardiovascular disease. In addition, we have previously shown that Arg109 and Arg223 homozygotes displayed lower intima-media thickness in our well-defined OPERA (Oulu Project Elucidating Risk of Atherosclerosis) study. This current research investigated the impact of these LEPR polymorphisms on cardiovascular events and related death as well as to total mortality in the 19-year follow-up of OPERA. Subjects were randomly selected, middle-aged drug-treated hypertensives and their age- and sex-matched control subjects recruited to the OPERA study between 1990 and 1993. Mortality and hospital events of 1045 subjects were followed up until 2009. A total of 151 coronary heart disease (CHD) and 211 cardiovascular disease (CVD) events or deaths including 58 CHD and 69 CVD deaths occurred. Furthermore, during this follow-up, a total of 165 subjects died. Logistic regression analysis was performed to assess the impact of Lys109Arg and Gln223Arg on the events and death. Further modeling was performed with Cox regression for Lys109Arg. The logistic regression analysis revealed a significant protective impact of Arg109Arg genotype on CHD (OR 0.433; CI 95% 0.217-0.863) and CVD (OR 0.540; CI 95% 0.309-0.942) events or death as well as on total mortality (OR 0.390; CI 95% 0.196-0.775) when adjusted with age, sex and study group. Even after further adjustment with BMI, smoking status, systolic blood pressure and low-density lipoprotein cholesterol, the protective effect of Arg109Arg on CHD events or death and total mortality still remained statistically significant (OR 0.463; CI 95% 0.230-0.931 and OR 0.442; CI 95% 0.218-0.896, respectively). Arg109Arg was also shown to confer protection against CHD mortality (HR 0.224; CI95% 0.055-0.919) and overall mortality (HR 0.413; CI95% 0.218-0.783) also in Cox regression analysis. In conclusion, the Arg109Arg genotype of LEPR seems to be protective from cardiovascular events and death and this phenomenon seems to be independent of the traditional risk factors for atherosclerosis.</AbstractText><CopyrightInformation>© 2013 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aijälä</LastName><ForeName>Meiju</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute of Clinical Medicine, Department of Internal Medicine and Biocenter Oulu, University of Oulu and Clinical Research Center, Oulu University Hospital, Oulu, Finland. Electronic address: meiju.aijala@oulu.fi.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Santaniemi</LastName><ForeName>Merja</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Bloigu</LastName><ForeName>Risto</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Kesäniemi</LastName><ForeName>Y Antero</ForeName><Initials>YA</Initials></Author><Author ValidYN="Y"><LastName>Ukkola</LastName><ForeName>Olavi</ForeName><Initials>O</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>10</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Gene</MedlineTA><NlmUniqueID>7706761</NlmUniqueID><ISSNLinking>0378-1119</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054411">Receptors, Leptin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C515448">leptin receptor, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>94ZLA3W45F</RegistryNumber><NameOfSubstance UI="D001120">Arginine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001120">Arginine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002318">Cardiovascular Diseases</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000401">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003327">Coronary Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005838">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D006720">Homozygote</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015994">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D054411">Receptors, Leptin</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ANOVA</Keyword><Keyword MajorTopicYN="N">Analysis of variance</Keyword><Keyword MajorTopicYN="N">Arg</Keyword><Keyword MajorTopicYN="N">Arginine</Keyword><Keyword MajorTopicYN="N">BMI</Keyword><Keyword MajorTopicYN="N">Body mass index</Keyword><Keyword MajorTopicYN="N">CHD</Keyword><Keyword MajorTopicYN="N">CI</Keyword><Keyword MajorTopicYN="N">CRH1</Keyword><Keyword MajorTopicYN="N">CVA</Keyword><Keyword MajorTopicYN="N">CVD</Keyword><Keyword MajorTopicYN="N">Cardiovascular disease</Keyword><Keyword MajorTopicYN="N">Cerebrovascular accident</Keyword><Keyword MajorTopicYN="N">Confidence interval</Keyword><Keyword MajorTopicYN="N">Coronary heart disease</Keyword><Keyword MajorTopicYN="N">Cytokine receptor homologous 1</Keyword><Keyword MajorTopicYN="N">F</Keyword><Keyword MajorTopicYN="N">Forward</Keyword><Keyword MajorTopicYN="N">Gln</Keyword><Keyword MajorTopicYN="N">Glutamine</Keyword><Keyword MajorTopicYN="N">HDL-C</Keyword><Keyword MajorTopicYN="N">HR</Keyword><Keyword MajorTopicYN="N">HWE</Keyword><Keyword MajorTopicYN="N">Hardy–Weinberg equilibrium</Keyword><Keyword MajorTopicYN="N">Hazard ratio</Keyword><Keyword MajorTopicYN="N">High-density lipoprotein cholesterol</Keyword><Keyword MajorTopicYN="N">ICD</Keyword><Keyword MajorTopicYN="N">International Classification of Diseases</Keyword><Keyword MajorTopicYN="N">LDL-C</Keyword><Keyword MajorTopicYN="N">LEPR</Keyword><Keyword MajorTopicYN="N">Lep</Keyword><Keyword MajorTopicYN="N">Leptin</Keyword><Keyword MajorTopicYN="N">Leptin receptor</Keyword><Keyword MajorTopicYN="N">Low-density lipoprotein cholesterol</Keyword><Keyword MajorTopicYN="N">Lys</Keyword><Keyword MajorTopicYN="N">Lysine</Keyword><Keyword MajorTopicYN="N">MI</Keyword><Keyword MajorTopicYN="N">Mortality</Keyword><Keyword MajorTopicYN="N">Myocardial infarction</Keyword><Keyword MajorTopicYN="N">OPERA</Keyword><Keyword MajorTopicYN="N">OR</Keyword><Keyword MajorTopicYN="N">Odds ratio</Keyword><Keyword MajorTopicYN="N">Oulu Project Elucidating Risk of Atherosclerosis</Keyword><Keyword MajorTopicYN="N">R</Keyword><Keyword MajorTopicYN="N">RIA</Keyword><Keyword MajorTopicYN="N">Radioimmunoassay</Keyword><Keyword MajorTopicYN="N">Reverse</Keyword><Keyword MajorTopicYN="N">SBP</Keyword><Keyword MajorTopicYN="N">SNP</Keyword><Keyword MajorTopicYN="N">Single nucleotide polymorphism</Keyword><Keyword MajorTopicYN="N">Systolic blood pressure</Keyword><Keyword MajorTopicYN="N">VLDL</Keyword><Keyword MajorTopicYN="N">Very low-density lipoprotein</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>8</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>9</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>10</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2013</Year><Month>10</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>10</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>10</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>1</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24140454</ArticleId><ArticleId IdType="pii">S0378-1119(13)01359-0</ArticleId><ArticleId IdType="doi">10.1016/j.gene.2013.10.003</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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