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Association between +45T>G adiponectin polymorphism gene and type 2 diabetes mellitus and metabolic syndrome in a Venezuelan population [version 1; peer review: 2 approved, 1 approved with reservations]
Background: Adiponectin (ADIPOQ) is a hormone primarily synthesized by adipocytes and encoded by the ADIPOQ gene, which exerts anti-inflammatory, antiatheratogenic and insulin sensitizing functions. It has been shown that its plasma concentrations are decreased in individuals with metabolic syndrome...
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Published in: | F1000 research 2019, Vol.8, p.292-292 |
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creator | Sánchez, María Patricia Prieto, Carem Mujica, Endrina Vergara, Kendry Valencia, Enifer Villalobos, Eudymar Medina, Mayerlim Parra, Michael D'Addosio, Rosanna Hoedebecke, Kyle Rodríguez, Johel E Bermudez, Valmore |
description | Background: Adiponectin (ADIPOQ) is a hormone primarily synthesized by adipocytes and encoded by the
ADIPOQ gene, which exerts anti-inflammatory, antiatheratogenic and insulin sensitizing functions. It has been shown that its plasma concentrations are decreased in individuals with metabolic syndrome (MS) and type 2 diabetes mellitus (DM2), which could be due to variations in the gene coding for this protein. The aim of this study was to detect the +45 T>G polymorphism of the
ADIPOQ gene in subjects with DM2 and MS in Maracaibo municipality, Zulia state, Venezuela.
Methods: A total of 90 subjects who attended the Center for Metabolic Endocrine Research "Dr. Félix Gómez" were enrolled for this study, 46 of which had MS-DM2 and 44 of which were healthy control individuals. Genomic DNA was extracted from blood samples and PCR-restriction fragment length polymorphism analysis was carried out for the promoter region of the
ADIPOQ gene. Likewise, the +45 T> G polymorphism was identified and correlated with MS and DM2 in the studied population.
Results: The most frequent allele in both groups was the T allele, and the predominant genotype was homozygous T/T (79%). Genotypes with heterozygous T/G and G/G homozygous polymorphism were more frequent in the control group than in the MS-DM2 group. Regarding the individuals with T/G and G/G genotypes, statistically significant lower mean values were found for fasting glucose, total cholesterol, triacylglycerides, abdominal circumference, and for the medians of systolic and diastolic blood pressure. Odds ratio were calculated for the presence or absence of MS and DM2.
Conclusions: The results suggested that the presence of the G allele exerts a protective effect on the carrier individuals, thus avoiding the appearance of the aforementioned metabolic alterations. |
doi_str_mv | 10.12688/f1000research.16890.1 |
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ADIPOQ gene, which exerts anti-inflammatory, antiatheratogenic and insulin sensitizing functions. It has been shown that its plasma concentrations are decreased in individuals with metabolic syndrome (MS) and type 2 diabetes mellitus (DM2), which could be due to variations in the gene coding for this protein. The aim of this study was to detect the +45 T>G polymorphism of the
ADIPOQ gene in subjects with DM2 and MS in Maracaibo municipality, Zulia state, Venezuela.
Methods: A total of 90 subjects who attended the Center for Metabolic Endocrine Research "Dr. Félix Gómez" were enrolled for this study, 46 of which had MS-DM2 and 44 of which were healthy control individuals. Genomic DNA was extracted from blood samples and PCR-restriction fragment length polymorphism analysis was carried out for the promoter region of the
ADIPOQ gene. Likewise, the +45 T> G polymorphism was identified and correlated with MS and DM2 in the studied population.
Results: The most frequent allele in both groups was the T allele, and the predominant genotype was homozygous T/T (79%). Genotypes with heterozygous T/G and G/G homozygous polymorphism were more frequent in the control group than in the MS-DM2 group. Regarding the individuals with T/G and G/G genotypes, statistically significant lower mean values were found for fasting glucose, total cholesterol, triacylglycerides, abdominal circumference, and for the medians of systolic and diastolic blood pressure. Odds ratio were calculated for the presence or absence of MS and DM2.
Conclusions: The results suggested that the presence of the G allele exerts a protective effect on the carrier individuals, thus avoiding the appearance of the aforementioned metabolic alterations.</description><identifier>ISSN: 2046-1402</identifier><identifier>EISSN: 2046-1402</identifier><identifier>DOI: 10.12688/f1000research.16890.1</identifier><identifier>PMID: 31131096</identifier><language>eng</language><publisher>England: Faculty of 1000 Ltd</publisher><subject>Adipocytes ; Adiponectin ; Alleles ; Blood pressure ; Cardiovascular disease ; Cholesterol ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Gene polymorphism ; Inflammation ; Insulin ; Insulin resistance ; Metabolic syndrome ; Mortality ; Population genetics ; Population studies ; Restriction fragment length polymorphism ; Statistical analysis ; Studies</subject><ispartof>F1000 research, 2019, Vol.8, p.292-292</ispartof><rights>Copyright: © 2019 Sánchez MP et al.</rights><rights>Copyright: © 2019 Sánchez MP et al. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright: © 2019 Sánchez MP et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4741-c69ce0061fad022b82cf22ce4a802741c8a96c2027e2b0407b59ad8ec28d064a3</citedby><cites>FETCH-LOGICAL-c4741-c69ce0061fad022b82cf22ce4a802741c8a96c2027e2b0407b59ad8ec28d064a3</cites><orcidid>0000-0002-0049-531X ; 0000-0002-3303-2258</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2233061844/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2233061844?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4022,25752,27922,27923,27924,37011,37012,44589,53790,53792,74897</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31131096$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sánchez, María Patricia</creatorcontrib><creatorcontrib>Prieto, Carem</creatorcontrib><creatorcontrib>Mujica, Endrina</creatorcontrib><creatorcontrib>Vergara, Kendry</creatorcontrib><creatorcontrib>Valencia, Enifer</creatorcontrib><creatorcontrib>Villalobos, Eudymar</creatorcontrib><creatorcontrib>Medina, Mayerlim</creatorcontrib><creatorcontrib>Parra, Michael</creatorcontrib><creatorcontrib>D'Addosio, Rosanna</creatorcontrib><creatorcontrib>Hoedebecke, Kyle</creatorcontrib><creatorcontrib>Rodríguez, Johel E</creatorcontrib><creatorcontrib>Bermudez, Valmore</creatorcontrib><title>Association between +45T>G adiponectin polymorphism gene and type 2 diabetes mellitus and metabolic syndrome in a Venezuelan population [version 1; peer review: 2 approved, 1 approved with reservations]</title><title>F1000 research</title><addtitle>F1000Res</addtitle><description>Background: Adiponectin (ADIPOQ) is a hormone primarily synthesized by adipocytes and encoded by the
ADIPOQ gene, which exerts anti-inflammatory, antiatheratogenic and insulin sensitizing functions. It has been shown that its plasma concentrations are decreased in individuals with metabolic syndrome (MS) and type 2 diabetes mellitus (DM2), which could be due to variations in the gene coding for this protein. The aim of this study was to detect the +45 T>G polymorphism of the
ADIPOQ gene in subjects with DM2 and MS in Maracaibo municipality, Zulia state, Venezuela.
Methods: A total of 90 subjects who attended the Center for Metabolic Endocrine Research "Dr. Félix Gómez" were enrolled for this study, 46 of which had MS-DM2 and 44 of which were healthy control individuals. Genomic DNA was extracted from blood samples and PCR-restriction fragment length polymorphism analysis was carried out for the promoter region of the
ADIPOQ gene. Likewise, the +45 T> G polymorphism was identified and correlated with MS and DM2 in the studied population.
Results: The most frequent allele in both groups was the T allele, and the predominant genotype was homozygous T/T (79%). Genotypes with heterozygous T/G and G/G homozygous polymorphism were more frequent in the control group than in the MS-DM2 group. Regarding the individuals with T/G and G/G genotypes, statistically significant lower mean values were found for fasting glucose, total cholesterol, triacylglycerides, abdominal circumference, and for the medians of systolic and diastolic blood pressure. Odds ratio were calculated for the presence or absence of MS and DM2.
Conclusions: The results suggested that the presence of the G allele exerts a protective effect on the carrier individuals, thus avoiding the appearance of the aforementioned metabolic alterations.</description><subject>Adipocytes</subject><subject>Adiponectin</subject><subject>Alleles</subject><subject>Blood pressure</subject><subject>Cardiovascular disease</subject><subject>Cholesterol</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Gene polymorphism</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Metabolic syndrome</subject><subject>Mortality</subject><subject>Population genetics</subject><subject>Population studies</subject><subject>Restriction fragment length polymorphism</subject><subject>Statistical analysis</subject><subject>Studies</subject><issn>2046-1402</issn><issn>2046-1402</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kt9u0zAUxiMEYtPYK0yWuEFiHf5XNxnSpGmCMWkSN4MbhKwT-6R1lcTBTlqVR-SpcNpRVi648ief7_vZPj5ZdsboBeMqz99VjFIaMCIEs7hgKi9S5Vl2zKlUEyYpf_5EH2WnMS5TgBaFUHz2MjsSjAlGC3Wc_bqO0RsHvfMtKbFfI7bkrZw-XN0SsK7zLZretaTz9abxoVu42JA5tkigtaTfdEg4sQ5SFCNpsK5dP8RtscEeSl87Q-KmtcE3SBIIyNeU_jlgDSO1G-rd2d9WGOIo2HvSIQYScOVwfZnw0HXBr9CeE7bXZO36BRlbEFZbQPz-KntRQR3x9HE9yb58_PBw82ly__n27ub6fmLkTLKJUYVBShWrwFLOy5ybinODEnLKk8HkUCjDk0ZeUkln5bQAm6PhuaVKgjjJ7nZc62Gpu-AaCBvtwenthg9zDaF3pkbNSmk4q3IQYiQnCkytokLYgnOc2cS62rG6oWzQGmz7APUB9LDSuoWe-5VWU0EVnSbAm0dA8D8GjL1uXDTpG6BFP0TNueCM00KM1tf_WJd-CG1q1ehKOJZLmVxq5zLBxxiw2l-GUb2dPn0wfXo7fZql4NnTp-xjf2YtGS53hgrMUPebkaL_Yv5P_w20Fe49</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Sánchez, María Patricia</creator><creator>Prieto, Carem</creator><creator>Mujica, Endrina</creator><creator>Vergara, Kendry</creator><creator>Valencia, Enifer</creator><creator>Villalobos, Eudymar</creator><creator>Medina, Mayerlim</creator><creator>Parra, Michael</creator><creator>D'Addosio, Rosanna</creator><creator>Hoedebecke, Kyle</creator><creator>Rodríguez, Johel E</creator><creator>Bermudez, Valmore</creator><general>Faculty of 1000 Ltd</general><general>F1000 Research Limited</general><general>F1000 Research Ltd</general><scope>C-E</scope><scope>CH4</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88I</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0049-531X</orcidid><orcidid>https://orcid.org/0000-0002-3303-2258</orcidid></search><sort><creationdate>2019</creationdate><title>Association between +45T>G adiponectin polymorphism gene and type 2 diabetes mellitus and metabolic syndrome in a Venezuelan population [version 1; peer review: 2 approved, 1 approved with reservations]</title><author>Sánchez, María Patricia ; Prieto, Carem ; Mujica, Endrina ; Vergara, Kendry ; Valencia, Enifer ; Villalobos, Eudymar ; Medina, Mayerlim ; Parra, Michael ; D'Addosio, Rosanna ; Hoedebecke, Kyle ; Rodríguez, Johel E ; Bermudez, Valmore</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4741-c69ce0061fad022b82cf22ce4a802741c8a96c2027e2b0407b59ad8ec28d064a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adipocytes</topic><topic>Adiponectin</topic><topic>Alleles</topic><topic>Blood pressure</topic><topic>Cardiovascular disease</topic><topic>Cholesterol</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Gene polymorphism</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Metabolic syndrome</topic><topic>Mortality</topic><topic>Population genetics</topic><topic>Population studies</topic><topic>Restriction fragment length polymorphism</topic><topic>Statistical analysis</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sánchez, María Patricia</creatorcontrib><creatorcontrib>Prieto, Carem</creatorcontrib><creatorcontrib>Mujica, Endrina</creatorcontrib><creatorcontrib>Vergara, Kendry</creatorcontrib><creatorcontrib>Valencia, Enifer</creatorcontrib><creatorcontrib>Villalobos, Eudymar</creatorcontrib><creatorcontrib>Medina, Mayerlim</creatorcontrib><creatorcontrib>Parra, Michael</creatorcontrib><creatorcontrib>D'Addosio, Rosanna</creatorcontrib><creatorcontrib>Hoedebecke, Kyle</creatorcontrib><creatorcontrib>Rodríguez, Johel E</creatorcontrib><creatorcontrib>Bermudez, Valmore</creatorcontrib><collection>F1000Research</collection><collection>Faculty of 1000</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>F1000 research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sánchez, María Patricia</au><au>Prieto, Carem</au><au>Mujica, Endrina</au><au>Vergara, Kendry</au><au>Valencia, Enifer</au><au>Villalobos, Eudymar</au><au>Medina, Mayerlim</au><au>Parra, Michael</au><au>D'Addosio, Rosanna</au><au>Hoedebecke, Kyle</au><au>Rodríguez, Johel E</au><au>Bermudez, Valmore</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association between +45T>G adiponectin polymorphism gene and type 2 diabetes mellitus and metabolic syndrome in a Venezuelan population [version 1; peer review: 2 approved, 1 approved with reservations]</atitle><jtitle>F1000 research</jtitle><addtitle>F1000Res</addtitle><date>2019</date><risdate>2019</risdate><volume>8</volume><spage>292</spage><epage>292</epage><pages>292-292</pages><issn>2046-1402</issn><eissn>2046-1402</eissn><abstract>Background: Adiponectin (ADIPOQ) is a hormone primarily synthesized by adipocytes and encoded by the
ADIPOQ gene, which exerts anti-inflammatory, antiatheratogenic and insulin sensitizing functions. It has been shown that its plasma concentrations are decreased in individuals with metabolic syndrome (MS) and type 2 diabetes mellitus (DM2), which could be due to variations in the gene coding for this protein. The aim of this study was to detect the +45 T>G polymorphism of the
ADIPOQ gene in subjects with DM2 and MS in Maracaibo municipality, Zulia state, Venezuela.
Methods: A total of 90 subjects who attended the Center for Metabolic Endocrine Research "Dr. Félix Gómez" were enrolled for this study, 46 of which had MS-DM2 and 44 of which were healthy control individuals. Genomic DNA was extracted from blood samples and PCR-restriction fragment length polymorphism analysis was carried out for the promoter region of the
ADIPOQ gene. Likewise, the +45 T> G polymorphism was identified and correlated with MS and DM2 in the studied population.
Results: The most frequent allele in both groups was the T allele, and the predominant genotype was homozygous T/T (79%). Genotypes with heterozygous T/G and G/G homozygous polymorphism were more frequent in the control group than in the MS-DM2 group. Regarding the individuals with T/G and G/G genotypes, statistically significant lower mean values were found for fasting glucose, total cholesterol, triacylglycerides, abdominal circumference, and for the medians of systolic and diastolic blood pressure. Odds ratio were calculated for the presence or absence of MS and DM2.
Conclusions: The results suggested that the presence of the G allele exerts a protective effect on the carrier individuals, thus avoiding the appearance of the aforementioned metabolic alterations.</abstract><cop>England</cop><pub>Faculty of 1000 Ltd</pub><pmid>31131096</pmid><doi>10.12688/f1000research.16890.1</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-0049-531X</orcidid><orcidid>https://orcid.org/0000-0002-3303-2258</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adipocytes Adiponectin Alleles Blood pressure Cardiovascular disease Cholesterol Diabetes mellitus Diabetes mellitus (non-insulin dependent) Gene polymorphism Inflammation Insulin Insulin resistance Metabolic syndrome Mortality Population genetics Population studies Restriction fragment length polymorphism Statistical analysis Studies |
title | Association between +45T>G adiponectin polymorphism gene and type 2 diabetes mellitus and metabolic syndrome in a Venezuelan population [version 1; peer review: 2 approved, 1 approved with reservations] |
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