Genetic variant of the renin-angiotensin system and prevalence of type 2 diabetes mellitus: a modest but significant effect of aldosterone synthase
Recent genome-wide association studies have identified multiple variants that confer risk of type 2 diabetes mellitus (DM). However, established associations explain only a part of the heritability. Thus, even at the genome-wide association studies era, candidate gene approach should be still useful...
Gespeichert in:
| Veröffentlicht in: | Acta diabetologica 2014-08, Vol.51 (4), p.595-599 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 599 |
|---|---|
| container_issue | 4 |
| container_start_page | 595 |
| container_title | Acta diabetologica |
| container_volume | 51 |
| creator | Ichikawa, Mai Konoshita, Tadashi Nakaya, Takahiro Yamamoto, Katsushi Yamada, Mika Sato, Satsuki Imagawa, Michiko Makino, Yasukazu Fujii, Miki Zenimaru, Yasuo Arakawa, Kenichiro Suzuki, Jinya Ishizuka, Tamotsu Nakamura, Hiroyuki |
| description | Recent genome-wide association studies have identified multiple variants that confer risk of type 2 diabetes mellitus (DM). However, established associations explain only a part of the heritability. Thus, even at the genome-wide association studies era, candidate gene approach should be still useful. Recent interventional studies against the renin-angiotensin system (RAS) showed reduction in new onset of DM, implying the system is involved in the onset. We substantiated the hypothesis that genetic variants of RAS have significant association with prevalence of DM. We enrolled to the study consecutive 782 subjects who had consulted our hospitals for mainly lifestyle related diseases. They consisted of 282 (36.1 %) diabetes cases. Genotypes were assayed with genomic DNA for conventional four genes of the RAS, i.e., angiotensin converting enzyme (ACE) insertion/deletion variant, angiotensinogen (AGT) M235T variant, angiotensin II type I receptor (AT1) A1166C variant, and aldosterone synthase (CYP11B2) C-344T variant. Association between the genetic variants of the RAS and prevalence of type 2 DM was tested. A significant association of DM and CYP11B2 genotype was obtained. There was no significant association between DM and ACE, AGT and AT1 variants. A multivariate logistic regression showed that age, gender, and CYP11B2 genotype were independent factors for association to diabetes, the DM risk of CC/CT to TT being 1.40 (95 % CI 1.04–1.90,
p
= 0.029). Thus, it is concluded that a genetic variant of the RAS should have a modest but significant impact on the onset of type 2 diabetes mellitus. |
| doi_str_mv | 10.1007/s00592-014-0561-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4127438</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3398090291</sourcerecordid><originalsourceid>FETCH-LOGICAL-c639t-49bf7d3ccd98efa9cbabb6a7b1a9253971071dfbc7b250549c7dcf0180430f703</originalsourceid><addsrcrecordid>eNqNks2KFDEUhQtRnHb0AdxIwI2b0puf6lRcCMOgozDgRtchlbrpzlCVtElqoJ_DFzbdPQ6jILjKIt89557LaZqXFN5SAPkuA3SKtUBFC92atvJRs6KCs7ZjnD9uVqAEtJ1g6qx5lvMNAGWS90-bMyY6oQQVq-bnFQYs3pJbk7wJhURHyhZJwuBDa8LGx4Ih-0DyPheciQkj2SW8NRMGi0d8v0PCyOjNgAUzmXGafFnye2LIHEfMhQxLIdlvgnfeHkzQObRHLzONseqmGLA6hLI1GZ83T5yZMr64e8-b758-frv83F5_vfpyeXHd2jVXpRVqcHLk1o6qR2eUHcwwrI0cqFGs40pSkHR0g5UD66AGtnK0DmgPgoOTwM-bDyfd3TLMOFoMJZlJ75KfTdrraLz-8yf4rd7EWy3qHQXvq8CbO4EUfyw1qJ59tjW-CRiXrGndUylg9D_QrmM9KOgPa73-C72JSwr1EkeK8w56Wil6omyKOSd093tT0Id26FM7dG2HPrRDyzrz6mHg-4nfdagAOwG5foUNpgfW_1T9BaVxyFc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1552335081</pqid></control><display><type>article</type><title>Genetic variant of the renin-angiotensin system and prevalence of type 2 diabetes mellitus: a modest but significant effect of aldosterone synthase</title><source>MEDLINE</source><source>Springer Journals</source><creator>Ichikawa, Mai ; Konoshita, Tadashi ; Nakaya, Takahiro ; Yamamoto, Katsushi ; Yamada, Mika ; Sato, Satsuki ; Imagawa, Michiko ; Makino, Yasukazu ; Fujii, Miki ; Zenimaru, Yasuo ; Arakawa, Kenichiro ; Suzuki, Jinya ; Ishizuka, Tamotsu ; Nakamura, Hiroyuki</creator><creatorcontrib>Ichikawa, Mai ; Konoshita, Tadashi ; Nakaya, Takahiro ; Yamamoto, Katsushi ; Yamada, Mika ; Sato, Satsuki ; Imagawa, Michiko ; Makino, Yasukazu ; Fujii, Miki ; Zenimaru, Yasuo ; Arakawa, Kenichiro ; Suzuki, Jinya ; Ishizuka, Tamotsu ; Nakamura, Hiroyuki</creatorcontrib><description>Recent genome-wide association studies have identified multiple variants that confer risk of type 2 diabetes mellitus (DM). However, established associations explain only a part of the heritability. Thus, even at the genome-wide association studies era, candidate gene approach should be still useful. Recent interventional studies against the renin-angiotensin system (RAS) showed reduction in new onset of DM, implying the system is involved in the onset. We substantiated the hypothesis that genetic variants of RAS have significant association with prevalence of DM. We enrolled to the study consecutive 782 subjects who had consulted our hospitals for mainly lifestyle related diseases. They consisted of 282 (36.1 %) diabetes cases. Genotypes were assayed with genomic DNA for conventional four genes of the RAS, i.e., angiotensin converting enzyme (ACE) insertion/deletion variant, angiotensinogen (AGT) M235T variant, angiotensin II type I receptor (AT1) A1166C variant, and aldosterone synthase (CYP11B2) C-344T variant. Association between the genetic variants of the RAS and prevalence of type 2 DM was tested. A significant association of DM and CYP11B2 genotype was obtained. There was no significant association between DM and ACE, AGT and AT1 variants. A multivariate logistic regression showed that age, gender, and CYP11B2 genotype were independent factors for association to diabetes, the DM risk of CC/CT to TT being 1.40 (95 % CI 1.04–1.90,
p
= 0.029). Thus, it is concluded that a genetic variant of the RAS should have a modest but significant impact on the onset of type 2 diabetes mellitus.</description><identifier>ISSN: 0940-5429</identifier><identifier>EISSN: 1432-5233</identifier><identifier>DOI: 10.1007/s00592-014-0561-7</identifier><identifier>PMID: 24549414</identifier><identifier>CODEN: ACDAEZ</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Aged ; Aged, 80 and over ; Angiotensinogen - genetics ; Cytochrome P-450 CYP11B2 - genetics ; Cytochrome P-450 CYP11B2 - metabolism ; Diabetes ; Diabetes Mellitus, Type 2 - enzymology ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Genetics ; Genotype ; Health risk assessment ; Humans ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Middle Aged ; Original ; Original Article ; Peptidyl-Dipeptidase A - genetics ; Polymorphism, Genetic ; Renin-Angiotensin System</subject><ispartof>Acta diabetologica, 2014-08, Vol.51 (4), p.595-599</ispartof><rights>The Author(s) 2014</rights><rights>Springer-Verlag Italia 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c639t-49bf7d3ccd98efa9cbabb6a7b1a9253971071dfbc7b250549c7dcf0180430f703</citedby><cites>FETCH-LOGICAL-c639t-49bf7d3ccd98efa9cbabb6a7b1a9253971071dfbc7b250549c7dcf0180430f703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00592-014-0561-7$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00592-014-0561-7$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24549414$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ichikawa, Mai</creatorcontrib><creatorcontrib>Konoshita, Tadashi</creatorcontrib><creatorcontrib>Nakaya, Takahiro</creatorcontrib><creatorcontrib>Yamamoto, Katsushi</creatorcontrib><creatorcontrib>Yamada, Mika</creatorcontrib><creatorcontrib>Sato, Satsuki</creatorcontrib><creatorcontrib>Imagawa, Michiko</creatorcontrib><creatorcontrib>Makino, Yasukazu</creatorcontrib><creatorcontrib>Fujii, Miki</creatorcontrib><creatorcontrib>Zenimaru, Yasuo</creatorcontrib><creatorcontrib>Arakawa, Kenichiro</creatorcontrib><creatorcontrib>Suzuki, Jinya</creatorcontrib><creatorcontrib>Ishizuka, Tamotsu</creatorcontrib><creatorcontrib>Nakamura, Hiroyuki</creatorcontrib><title>Genetic variant of the renin-angiotensin system and prevalence of type 2 diabetes mellitus: a modest but significant effect of aldosterone synthase</title><title>Acta diabetologica</title><addtitle>Acta Diabetol</addtitle><addtitle>Acta Diabetol</addtitle><description>Recent genome-wide association studies have identified multiple variants that confer risk of type 2 diabetes mellitus (DM). However, established associations explain only a part of the heritability. Thus, even at the genome-wide association studies era, candidate gene approach should be still useful. Recent interventional studies against the renin-angiotensin system (RAS) showed reduction in new onset of DM, implying the system is involved in the onset. We substantiated the hypothesis that genetic variants of RAS have significant association with prevalence of DM. We enrolled to the study consecutive 782 subjects who had consulted our hospitals for mainly lifestyle related diseases. They consisted of 282 (36.1 %) diabetes cases. Genotypes were assayed with genomic DNA for conventional four genes of the RAS, i.e., angiotensin converting enzyme (ACE) insertion/deletion variant, angiotensinogen (AGT) M235T variant, angiotensin II type I receptor (AT1) A1166C variant, and aldosterone synthase (CYP11B2) C-344T variant. Association between the genetic variants of the RAS and prevalence of type 2 DM was tested. A significant association of DM and CYP11B2 genotype was obtained. There was no significant association between DM and ACE, AGT and AT1 variants. A multivariate logistic regression showed that age, gender, and CYP11B2 genotype were independent factors for association to diabetes, the DM risk of CC/CT to TT being 1.40 (95 % CI 1.04–1.90,
p
= 0.029). Thus, it is concluded that a genetic variant of the RAS should have a modest but significant impact on the onset of type 2 diabetes mellitus.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Angiotensinogen - genetics</subject><subject>Cytochrome P-450 CYP11B2 - genetics</subject><subject>Cytochrome P-450 CYP11B2 - metabolism</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - enzymology</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Variation</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Middle Aged</subject><subject>Original</subject><subject>Original Article</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Polymorphism, Genetic</subject><subject>Renin-Angiotensin System</subject><issn>0940-5429</issn><issn>1432-5233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNks2KFDEUhQtRnHb0AdxIwI2b0puf6lRcCMOgozDgRtchlbrpzlCVtElqoJ_DFzbdPQ6jILjKIt89557LaZqXFN5SAPkuA3SKtUBFC92atvJRs6KCs7ZjnD9uVqAEtJ1g6qx5lvMNAGWS90-bMyY6oQQVq-bnFQYs3pJbk7wJhURHyhZJwuBDa8LGx4Ih-0DyPheciQkj2SW8NRMGi0d8v0PCyOjNgAUzmXGafFnye2LIHEfMhQxLIdlvgnfeHkzQObRHLzONseqmGLA6hLI1GZ83T5yZMr64e8-b758-frv83F5_vfpyeXHd2jVXpRVqcHLk1o6qR2eUHcwwrI0cqFGs40pSkHR0g5UD66AGtnK0DmgPgoOTwM-bDyfd3TLMOFoMJZlJ75KfTdrraLz-8yf4rd7EWy3qHQXvq8CbO4EUfyw1qJ59tjW-CRiXrGndUylg9D_QrmM9KOgPa73-C72JSwr1EkeK8w56Wil6omyKOSd093tT0Id26FM7dG2HPrRDyzrz6mHg-4nfdagAOwG5foUNpgfW_1T9BaVxyFc</recordid><startdate>20140801</startdate><enddate>20140801</enddate><creator>Ichikawa, Mai</creator><creator>Konoshita, Tadashi</creator><creator>Nakaya, Takahiro</creator><creator>Yamamoto, Katsushi</creator><creator>Yamada, Mika</creator><creator>Sato, Satsuki</creator><creator>Imagawa, Michiko</creator><creator>Makino, Yasukazu</creator><creator>Fujii, Miki</creator><creator>Zenimaru, Yasuo</creator><creator>Arakawa, Kenichiro</creator><creator>Suzuki, Jinya</creator><creator>Ishizuka, Tamotsu</creator><creator>Nakamura, Hiroyuki</creator><general>Springer Milan</general><general>Springer Nature B.V</general><scope>C6C</scope><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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20140801</creationdate><title>Genetic variant of the renin-angiotensin system and prevalence of type 2 diabetes mellitus: a modest but significant effect of aldosterone synthase</title><author>Ichikawa, Mai ; Konoshita, Tadashi ; Nakaya, Takahiro ; Yamamoto, Katsushi ; Yamada, Mika ; Sato, Satsuki ; Imagawa, Michiko ; Makino, Yasukazu ; Fujii, Miki ; Zenimaru, Yasuo ; Arakawa, Kenichiro ; Suzuki, Jinya ; Ishizuka, Tamotsu ; Nakamura, Hiroyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c639t-49bf7d3ccd98efa9cbabb6a7b1a9253971071dfbc7b250549c7dcf0180430f703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Angiotensinogen - genetics</topic><topic>Cytochrome P-450 CYP11B2 - genetics</topic><topic>Cytochrome P-450 CYP11B2 - metabolism</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - enzymology</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic Variation</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Health risk assessment</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Middle Aged</topic><topic>Original</topic><topic>Original Article</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Polymorphism, Genetic</topic><topic>Renin-Angiotensin System</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ichikawa, Mai</creatorcontrib><creatorcontrib>Konoshita, Tadashi</creatorcontrib><creatorcontrib>Nakaya, Takahiro</creatorcontrib><creatorcontrib>Yamamoto, Katsushi</creatorcontrib><creatorcontrib>Yamada, Mika</creatorcontrib><creatorcontrib>Sato, Satsuki</creatorcontrib><creatorcontrib>Imagawa, Michiko</creatorcontrib><creatorcontrib>Makino, Yasukazu</creatorcontrib><creatorcontrib>Fujii, Miki</creatorcontrib><creatorcontrib>Zenimaru, Yasuo</creatorcontrib><creatorcontrib>Arakawa, Kenichiro</creatorcontrib><creatorcontrib>Suzuki, Jinya</creatorcontrib><creatorcontrib>Ishizuka, Tamotsu</creatorcontrib><creatorcontrib>Nakamura, Hiroyuki</creatorcontrib><collection>SpringerOpen</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta diabetologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ichikawa, Mai</au><au>Konoshita, Tadashi</au><au>Nakaya, Takahiro</au><au>Yamamoto, Katsushi</au><au>Yamada, Mika</au><au>Sato, Satsuki</au><au>Imagawa, Michiko</au><au>Makino, Yasukazu</au><au>Fujii, Miki</au><au>Zenimaru, Yasuo</au><au>Arakawa, Kenichiro</au><au>Suzuki, Jinya</au><au>Ishizuka, Tamotsu</au><au>Nakamura, Hiroyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic variant of the renin-angiotensin system and prevalence of type 2 diabetes mellitus: a modest but significant effect of aldosterone synthase</atitle><jtitle>Acta diabetologica</jtitle><stitle>Acta Diabetol</stitle><addtitle>Acta Diabetol</addtitle><date>2014-08-01</date><risdate>2014</risdate><volume>51</volume><issue>4</issue><spage>595</spage><epage>599</epage><pages>595-599</pages><issn>0940-5429</issn><eissn>1432-5233</eissn><coden>ACDAEZ</coden><abstract>Recent genome-wide association studies have identified multiple variants that confer risk of type 2 diabetes mellitus (DM). However, established associations explain only a part of the heritability. Thus, even at the genome-wide association studies era, candidate gene approach should be still useful. Recent interventional studies against the renin-angiotensin system (RAS) showed reduction in new onset of DM, implying the system is involved in the onset. We substantiated the hypothesis that genetic variants of RAS have significant association with prevalence of DM. We enrolled to the study consecutive 782 subjects who had consulted our hospitals for mainly lifestyle related diseases. They consisted of 282 (36.1 %) diabetes cases. Genotypes were assayed with genomic DNA for conventional four genes of the RAS, i.e., angiotensin converting enzyme (ACE) insertion/deletion variant, angiotensinogen (AGT) M235T variant, angiotensin II type I receptor (AT1) A1166C variant, and aldosterone synthase (CYP11B2) C-344T variant. Association between the genetic variants of the RAS and prevalence of type 2 DM was tested. A significant association of DM and CYP11B2 genotype was obtained. There was no significant association between DM and ACE, AGT and AT1 variants. A multivariate logistic regression showed that age, gender, and CYP11B2 genotype were independent factors for association to diabetes, the DM risk of CC/CT to TT being 1.40 (95 % CI 1.04–1.90,
p
= 0.029). Thus, it is concluded that a genetic variant of the RAS should have a modest but significant impact on the onset of type 2 diabetes mellitus.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>24549414</pmid><doi>10.1007/s00592-014-0561-7</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0940-5429 |
| ispartof | Acta diabetologica, 2014-08, Vol.51 (4), p.595-599 |
| issn | 0940-5429 1432-5233 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4127438 |
| source | MEDLINE; Springer Journals |
| subjects | Aged Aged, 80 and over Angiotensinogen - genetics Cytochrome P-450 CYP11B2 - genetics Cytochrome P-450 CYP11B2 - metabolism Diabetes Diabetes Mellitus, Type 2 - enzymology Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Female Genetic Predisposition to Disease Genetic Variation Genetics Genotype Health risk assessment Humans Internal Medicine Male Medicine Medicine & Public Health Metabolic Diseases Middle Aged Original Original Article Peptidyl-Dipeptidase A - genetics Polymorphism, Genetic Renin-Angiotensin System |
| title | Genetic variant of the renin-angiotensin system and prevalence of type 2 diabetes mellitus: a modest but significant effect of aldosterone synthase |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T18%3A48%3A57IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Genetic%20variant%20of%20the%20renin-angiotensin%20system%20and%20prevalence%20of%20type%202%20diabetes%20mellitus:%20a%20modest%20but%20significant%20effect%20of%20aldosterone%20synthase&rft.jtitle=Acta%20diabetologica&rft.au=Ichikawa,%20Mai&rft.date=2014-08-01&rft.volume=51&rft.issue=4&rft.spage=595&rft.epage=599&rft.pages=595-599&rft.issn=0940-5429&rft.eissn=1432-5233&rft.coden=ACDAEZ&rft_id=info:doi/10.1007/s00592-014-0561-7&rft_dat=%3Cproquest_pubme%3E3398090291%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1552335081&rft_id=info:pmid/24549414&rfr_iscdi=true |