Lack of Association Between Type 2 Diabetes and the 3673G / A and 9041G / A Gene Variants of Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1)

The vitamin K epoxide reductase complex subunit 1 (VKORC1) gene is expressed in many tissue types, and encodes the VKORC1 protein, which is a key enzyme in the vitamin K cycle. Although researchers have focused on the effects of vitamin K on glucose metabolism, and on its role in the development of...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:International journal for vitamin and nutrition research 2016-06, Vol.86 (3-4), p.1-139
Hauptverfasser: Ozbayer, Cansu, Kurt, Hulyam, Nur Kebapci, Medine, Turgut Cosan, Didem, Colak, Ertugrul, Veysi Gunes, Hasan, Degirmenci, Irfan
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 139
container_issue 3-4
container_start_page 1
container_title International journal for vitamin and nutrition research
container_volume 86
creator Ozbayer, Cansu
Kurt, Hulyam
Nur Kebapci, Medine
Turgut Cosan, Didem
Colak, Ertugrul
Veysi Gunes, Hasan
Degirmenci, Irfan
description The vitamin K epoxide reductase complex subunit 1 (VKORC1) gene is expressed in many tissue types, and encodes the VKORC1 protein, which is a key enzyme in the vitamin K cycle. Although researchers have focused on the effects of vitamin K on glucose metabolism, and on its role in the development of type 2 diabetes (T2DM), no consensus has yet been reached. Therefore, here we aimed to investigate the association between VKORC1 variants and the risk of T2DM. The 3673G / A (rs9923231) and 9041G / A (rs7294) VKORC1 variants were investigated by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 100 control individuals and 100 patients with T2DM. The genomic regions were amplified by PCR; amplicons were digested using the AciI and NciI enzymes and visualized by agarose gel electrophoresis. The genotype frequencies of the 3673G / A variants were GG (22%), GA (56%), and AA (22%) in the control group and GG (19%), GA (52%), and AA (29%) in patients with T2DM (p > 0.05). The genotype frequencies of the 9041G / A variants were GG (37%), GA (53%), and AA (10%) in the control group and GG (46%), GA (45%), and AA (9%) in patients with T2DM (p > 0.05). In conclusion, we found no significant correlation between the control group and patients with T2DM, with regard to the different genetic models of the 3673G / A and 9041G / A variants. These data suggest that these VKORC1 gene variants may not be linked to T2DM.
doi_str_mv 10.1024/0300-9831/a000302
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2007424597</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2007424597</sourcerecordid><originalsourceid>FETCH-LOGICAL-c253t-3ba26ce2ac314512353fd3afc4be73c7920a8e361c5cae1569f22e8b44ab9d3e3</originalsourceid><addsrcrecordid>eNo9UUlOw0AQHCEQhOUBXFAf4WAym7djCBAQkSKx5Gq1x20xEC94xgLewYdJSMipVV3LoYqxU8EvBZd6yBXnQZooMUTOl0DusIGIIh3IRIpdNtjyB-zQubelJBaJ3mcHMtVRGiViwH6maN6hKWHkXGMsetvUcEX-k6iG5--WQMK1xZw8OcC6AP9KoKJYTWAIo79PyrVYownVBHPsLNberULn1mNla3iAm7b5sgXBIxW98egIxk3VLugLnvq8r60HAefzh9njWFwcs70SF45ONveIvdzePI_vgulscj8eTQMjQ-UDlaOMDEk0SuhQSBWqslBYGp1TrEycSo4JqUiY0CCJMEpLKSnJtcY8LRSpI3a-zm275qMn57PKOkOLBdbU9C6TnMda6jCNl1Kxlpquca6jMms7W2H3nQmerbbIVl1nq66zzRZLz9kmvs8rKraO__LVL2IpgD0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2007424597</pqid></control><display><type>article</type><title>Lack of Association Between Type 2 Diabetes and the 3673G / A and 9041G / A Gene Variants of Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1)</title><source>Hogrefe eContent</source><source>Alma/SFX Local Collection</source><creator>Ozbayer, Cansu ; Kurt, Hulyam ; Nur Kebapci, Medine ; Turgut Cosan, Didem ; Colak, Ertugrul ; Veysi Gunes, Hasan ; Degirmenci, Irfan</creator><creatorcontrib>Ozbayer, Cansu ; Kurt, Hulyam ; Nur Kebapci, Medine ; Turgut Cosan, Didem ; Colak, Ertugrul ; Veysi Gunes, Hasan ; Degirmenci, Irfan</creatorcontrib><description>The vitamin K epoxide reductase complex subunit 1 (VKORC1) gene is expressed in many tissue types, and encodes the VKORC1 protein, which is a key enzyme in the vitamin K cycle. Although researchers have focused on the effects of vitamin K on glucose metabolism, and on its role in the development of type 2 diabetes (T2DM), no consensus has yet been reached. Therefore, here we aimed to investigate the association between VKORC1 variants and the risk of T2DM. The 3673G / A (rs9923231) and 9041G / A (rs7294) VKORC1 variants were investigated by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 100 control individuals and 100 patients with T2DM. The genomic regions were amplified by PCR; amplicons were digested using the AciI and NciI enzymes and visualized by agarose gel electrophoresis. The genotype frequencies of the 3673G / A variants were GG (22%), GA (56%), and AA (22%) in the control group and GG (19%), GA (52%), and AA (29%) in patients with T2DM (p &gt; 0.05). The genotype frequencies of the 9041G / A variants were GG (37%), GA (53%), and AA (10%) in the control group and GG (46%), GA (45%), and AA (9%) in patients with T2DM (p &gt; 0.05). In conclusion, we found no significant correlation between the control group and patients with T2DM, with regard to the different genetic models of the 3673G / A and 9041G / A variants. These data suggest that these VKORC1 gene variants may not be linked to T2DM.</description><identifier>ISSN: 0300-9831</identifier><identifier>EISSN: 1664-2821</identifier><identifier>DOI: 10.1024/0300-9831/a000302</identifier><identifier>PMID: 29469681</identifier><language>eng</language><publisher>Switzerland</publisher><ispartof>International journal for vitamin and nutrition research, 2016-06, Vol.86 (3-4), p.1-139</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29469681$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ozbayer, Cansu</creatorcontrib><creatorcontrib>Kurt, Hulyam</creatorcontrib><creatorcontrib>Nur Kebapci, Medine</creatorcontrib><creatorcontrib>Turgut Cosan, Didem</creatorcontrib><creatorcontrib>Colak, Ertugrul</creatorcontrib><creatorcontrib>Veysi Gunes, Hasan</creatorcontrib><creatorcontrib>Degirmenci, Irfan</creatorcontrib><title>Lack of Association Between Type 2 Diabetes and the 3673G / A and 9041G / A Gene Variants of Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1)</title><title>International journal for vitamin and nutrition research</title><addtitle>Int J Vitam Nutr Res</addtitle><description>The vitamin K epoxide reductase complex subunit 1 (VKORC1) gene is expressed in many tissue types, and encodes the VKORC1 protein, which is a key enzyme in the vitamin K cycle. Although researchers have focused on the effects of vitamin K on glucose metabolism, and on its role in the development of type 2 diabetes (T2DM), no consensus has yet been reached. Therefore, here we aimed to investigate the association between VKORC1 variants and the risk of T2DM. The 3673G / A (rs9923231) and 9041G / A (rs7294) VKORC1 variants were investigated by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 100 control individuals and 100 patients with T2DM. The genomic regions were amplified by PCR; amplicons were digested using the AciI and NciI enzymes and visualized by agarose gel electrophoresis. The genotype frequencies of the 3673G / A variants were GG (22%), GA (56%), and AA (22%) in the control group and GG (19%), GA (52%), and AA (29%) in patients with T2DM (p &gt; 0.05). The genotype frequencies of the 9041G / A variants were GG (37%), GA (53%), and AA (10%) in the control group and GG (46%), GA (45%), and AA (9%) in patients with T2DM (p &gt; 0.05). In conclusion, we found no significant correlation between the control group and patients with T2DM, with regard to the different genetic models of the 3673G / A and 9041G / A variants. These data suggest that these VKORC1 gene variants may not be linked to T2DM.</description><issn>0300-9831</issn><issn>1664-2821</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNo9UUlOw0AQHCEQhOUBXFAf4WAym7djCBAQkSKx5Gq1x20xEC94xgLewYdJSMipVV3LoYqxU8EvBZd6yBXnQZooMUTOl0DusIGIIh3IRIpdNtjyB-zQubelJBaJ3mcHMtVRGiViwH6maN6hKWHkXGMsetvUcEX-k6iG5--WQMK1xZw8OcC6AP9KoKJYTWAIo79PyrVYownVBHPsLNberULn1mNla3iAm7b5sgXBIxW98egIxk3VLugLnvq8r60HAefzh9njWFwcs70SF45ONveIvdzePI_vgulscj8eTQMjQ-UDlaOMDEk0SuhQSBWqslBYGp1TrEycSo4JqUiY0CCJMEpLKSnJtcY8LRSpI3a-zm275qMn57PKOkOLBdbU9C6TnMda6jCNl1Kxlpquca6jMms7W2H3nQmerbbIVl1nq66zzRZLz9kmvs8rKraO__LVL2IpgD0</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Ozbayer, Cansu</creator><creator>Kurt, Hulyam</creator><creator>Nur Kebapci, Medine</creator><creator>Turgut Cosan, Didem</creator><creator>Colak, Ertugrul</creator><creator>Veysi Gunes, Hasan</creator><creator>Degirmenci, Irfan</creator><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20160601</creationdate><title>Lack of Association Between Type 2 Diabetes and the 3673G / A and 9041G / A Gene Variants of Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1)</title><author>Ozbayer, Cansu ; Kurt, Hulyam ; Nur Kebapci, Medine ; Turgut Cosan, Didem ; Colak, Ertugrul ; Veysi Gunes, Hasan ; Degirmenci, Irfan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c253t-3ba26ce2ac314512353fd3afc4be73c7920a8e361c5cae1569f22e8b44ab9d3e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ozbayer, Cansu</creatorcontrib><creatorcontrib>Kurt, Hulyam</creatorcontrib><creatorcontrib>Nur Kebapci, Medine</creatorcontrib><creatorcontrib>Turgut Cosan, Didem</creatorcontrib><creatorcontrib>Colak, Ertugrul</creatorcontrib><creatorcontrib>Veysi Gunes, Hasan</creatorcontrib><creatorcontrib>Degirmenci, Irfan</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International journal for vitamin and nutrition research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ozbayer, Cansu</au><au>Kurt, Hulyam</au><au>Nur Kebapci, Medine</au><au>Turgut Cosan, Didem</au><au>Colak, Ertugrul</au><au>Veysi Gunes, Hasan</au><au>Degirmenci, Irfan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of Association Between Type 2 Diabetes and the 3673G / A and 9041G / A Gene Variants of Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1)</atitle><jtitle>International journal for vitamin and nutrition research</jtitle><addtitle>Int J Vitam Nutr Res</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>86</volume><issue>3-4</issue><spage>1</spage><epage>139</epage><pages>1-139</pages><issn>0300-9831</issn><eissn>1664-2821</eissn><abstract>The vitamin K epoxide reductase complex subunit 1 (VKORC1) gene is expressed in many tissue types, and encodes the VKORC1 protein, which is a key enzyme in the vitamin K cycle. Although researchers have focused on the effects of vitamin K on glucose metabolism, and on its role in the development of type 2 diabetes (T2DM), no consensus has yet been reached. Therefore, here we aimed to investigate the association between VKORC1 variants and the risk of T2DM. The 3673G / A (rs9923231) and 9041G / A (rs7294) VKORC1 variants were investigated by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 100 control individuals and 100 patients with T2DM. The genomic regions were amplified by PCR; amplicons were digested using the AciI and NciI enzymes and visualized by agarose gel electrophoresis. The genotype frequencies of the 3673G / A variants were GG (22%), GA (56%), and AA (22%) in the control group and GG (19%), GA (52%), and AA (29%) in patients with T2DM (p &gt; 0.05). The genotype frequencies of the 9041G / A variants were GG (37%), GA (53%), and AA (10%) in the control group and GG (46%), GA (45%), and AA (9%) in patients with T2DM (p &gt; 0.05). In conclusion, we found no significant correlation between the control group and patients with T2DM, with regard to the different genetic models of the 3673G / A and 9041G / A variants. These data suggest that these VKORC1 gene variants may not be linked to T2DM.</abstract><cop>Switzerland</cop><pmid>29469681</pmid><doi>10.1024/0300-9831/a000302</doi><tpages>7</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0300-9831
ispartof International journal for vitamin and nutrition research, 2016-06, Vol.86 (3-4), p.1-139
issn 0300-9831
1664-2821
language eng
recordid cdi_proquest_miscellaneous_2007424597
source Hogrefe eContent; Alma/SFX Local Collection
title Lack of Association Between Type 2 Diabetes and the 3673G / A and 9041G / A Gene Variants of Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1)
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T05%3A23%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Lack%20of%20Association%20Between%20Type%202%20Diabetes%20and%20the%203673G%20/%20A%20and%209041G%20/%20A%20Gene%20Variants%20of%20Vitamin%20K%20Epoxide%20Reductase%20Complex%20Subunit%201%20(VKORC1)&rft.jtitle=International%20journal%20for%20vitamin%20and%20nutrition%20research&rft.au=Ozbayer,%20Cansu&rft.date=2016-06-01&rft.volume=86&rft.issue=3-4&rft.spage=1&rft.epage=139&rft.pages=1-139&rft.issn=0300-9831&rft.eissn=1664-2821&rft_id=info:doi/10.1024/0300-9831/a000302&rft_dat=%3Cproquest_cross%3E2007424597%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2007424597&rft_id=info:pmid/29469681&rfr_iscdi=true