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Association of Omentin rs2274907 and FTO rs9939609 gene polymorphisms with insulin resistance in Iranian individuals with newly diagnosed type 2 diabetes
Insulin resistance (IR) and fat accumulation in visceral adipose tissue are key players in developing type 2 diabetes (T2D). Several adipose tissue derived-gene polymorphisms are related to higher body mass index (BMI), insulin resistance and T2D. The association of omentin rs2274907 (Val109Asp) and...
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Published in: | Lipids in health and disease 2019-06, Vol.18 (1), p.142-142, Article 142 |
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description | Insulin resistance (IR) and fat accumulation in visceral adipose tissue are key players in developing type 2 diabetes (T2D). Several adipose tissue derived-gene polymorphisms are related to higher body mass index (BMI), insulin resistance and T2D. The association of omentin rs2274907 (Val109Asp) and fat-mass and obesity-associated (FTO) rs9939609 gene polymorphisms with overweight/obesity and T2D is controversial. The aim of this study was to determine the association between omentin Val109Asp and FTO rs9939609 polymorphisms and insulin resistance in newly-diagnosed T2D patients.
The case-control study included 83 newly-diagnosed T2D patients and 85 healthy matched controls, aged 20-80 years. Fasting blood glucose and insulin levels were measured by the enzymatic method and enzyme-linked-immunosorbent assay, respectively. Insulin resistance was calculated using the homeostasis model assessment (HOMA) index. Genotyping was examined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).
There are significant differences between both omentin Val109Asp and FTO rs9939609 polymorphisms and studied individuals (P = 0.011 and P = 0.0001, respectively). Both genetic polymorphisms of omentin Val109Asp and FTO rs9939609 (T/A) are significantly related to higher HOMA index (P = 0.030 and P = 0.046, respectively). However, omentin Val109Asp polymorphism was only related to individuals who were overweight/obese. Additionally, both omentin Val109Asp and FTO rs9939609 polymorphisms were significantly positively correlated to familial history of diabetes (P = 0.046 and P = 0.024, respectively).
Omentin V109D and FTO rs9939609 genetic variations may change insulin metabolism and have key roles in developing T2D through insulin resistance. Thus, the evaluation of these polymorphic regions may be helpful for predicting type 2 diabetes. |
doi_str_mv | 10.1186/s12944-019-1085-5 |
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The case-control study included 83 newly-diagnosed T2D patients and 85 healthy matched controls, aged 20-80 years. Fasting blood glucose and insulin levels were measured by the enzymatic method and enzyme-linked-immunosorbent assay, respectively. Insulin resistance was calculated using the homeostasis model assessment (HOMA) index. Genotyping was examined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).
There are significant differences between both omentin Val109Asp and FTO rs9939609 polymorphisms and studied individuals (P = 0.011 and P = 0.0001, respectively). Both genetic polymorphisms of omentin Val109Asp and FTO rs9939609 (T/A) are significantly related to higher HOMA index (P = 0.030 and P = 0.046, respectively). However, omentin Val109Asp polymorphism was only related to individuals who were overweight/obese. Additionally, both omentin Val109Asp and FTO rs9939609 polymorphisms were significantly positively correlated to familial history of diabetes (P = 0.046 and P = 0.024, respectively).
Omentin V109D and FTO rs9939609 genetic variations may change insulin metabolism and have key roles in developing T2D through insulin resistance. Thus, the evaluation of these polymorphic regions may be helpful for predicting type 2 diabetes.</description><identifier>ISSN: 1476-511X</identifier><identifier>EISSN: 1476-511X</identifier><identifier>DOI: 10.1186/s12944-019-1085-5</identifier><identifier>PMID: 31200723</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adipose tissue ; Adult ; Aged ; Aged, 80 and over ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO ; Blood glucose ; Blood Glucose - metabolism ; Body Mass Index ; Body weight ; Cardiovascular disease ; Case-Control Studies ; Cholesterol ; Cytokines - genetics ; Deoxyribonucleic acid ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - diagnosis ; Diabetes Mellitus, Type 2 - genetics ; Diabetes therapy ; Diagnosis ; DNA ; Enzymes ; Fasting ; Fat mass-and obesity associated (FTO) ; Gene polymorphism ; Genes ; Genetic aspects ; Genetic diversity ; Genetic polymorphisms ; Genetic Predisposition to Disease - genetics ; Genetic research ; Genomes ; Genotyping ; Glucose ; GPI-Linked Proteins - genetics ; Homeostasis ; Humans ; Hyperglycemia ; Hypertension ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Insulin Resistance - physiology ; Iran ; Laboratories ; Lectins - genetics ; Metabolism ; Middle Aged ; Obesity ; Omentin ; Overweight ; Polymerase chain reaction ; Polymorphism ; Polymorphism, Restriction Fragment Length - genetics ; Polymorphism, Single Nucleotide - genetics ; Population ; Restriction fragment length polymorphism ; Studies ; Type 2 diabetes ; Young Adult</subject><ispartof>Lipids in health and disease, 2019-06, Vol.18 (1), p.142-142, Article 142</ispartof><rights>COPYRIGHT 2019 BioMed Central Ltd.</rights><rights>2019. This work is licensed 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>The Author(s). 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-fd870213edadfa1774e5baf9e482a9bbc5db11f1bcfde1eb7e1d118bea4d01c33</citedby><cites>FETCH-LOGICAL-c560t-fd870213edadfa1774e5baf9e482a9bbc5db11f1bcfde1eb7e1d118bea4d01c33</cites><orcidid>0000-0001-9520-1857</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6570836/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2243374636?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25733,27903,27904,36991,36992,44569,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31200723$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khoshi, Amirhosein</creatorcontrib><creatorcontrib>Bajestani, Mehdi Kaffash</creatorcontrib><creatorcontrib>Shakeri, Habibesadat</creatorcontrib><creatorcontrib>Goodarzi, Golnaz</creatorcontrib><creatorcontrib>Azizi, Fatemeh</creatorcontrib><title>Association of Omentin rs2274907 and FTO rs9939609 gene polymorphisms with insulin resistance in Iranian individuals with newly diagnosed type 2 diabetes</title><title>Lipids in health and disease</title><addtitle>Lipids Health Dis</addtitle><description>Insulin resistance (IR) and fat accumulation in visceral adipose tissue are key players in developing type 2 diabetes (T2D). Several adipose tissue derived-gene polymorphisms are related to higher body mass index (BMI), insulin resistance and T2D. The association of omentin rs2274907 (Val109Asp) and fat-mass and obesity-associated (FTO) rs9939609 gene polymorphisms with overweight/obesity and T2D is controversial. The aim of this study was to determine the association between omentin Val109Asp and FTO rs9939609 polymorphisms and insulin resistance in newly-diagnosed T2D patients.
The case-control study included 83 newly-diagnosed T2D patients and 85 healthy matched controls, aged 20-80 years. Fasting blood glucose and insulin levels were measured by the enzymatic method and enzyme-linked-immunosorbent assay, respectively. Insulin resistance was calculated using the homeostasis model assessment (HOMA) index. Genotyping was examined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).
There are significant differences between both omentin Val109Asp and FTO rs9939609 polymorphisms and studied individuals (P = 0.011 and P = 0.0001, respectively). Both genetic polymorphisms of omentin Val109Asp and FTO rs9939609 (T/A) are significantly related to higher HOMA index (P = 0.030 and P = 0.046, respectively). However, omentin Val109Asp polymorphism was only related to individuals who were overweight/obese. Additionally, both omentin Val109Asp and FTO rs9939609 polymorphisms were significantly positively correlated to familial history of diabetes (P = 0.046 and P = 0.024, respectively).
Omentin V109D and FTO rs9939609 genetic variations may change insulin metabolism and have key roles in developing T2D through insulin resistance. Thus, the evaluation of these polymorphic regions may be helpful for predicting type 2 diabetes.</description><subject>Adipose tissue</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alpha-Ketoglutarate-Dependent Dioxygenase FTO</subject><subject>Blood glucose</subject><subject>Blood Glucose - metabolism</subject><subject>Body Mass Index</subject><subject>Body weight</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Cholesterol</subject><subject>Cytokines - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - diagnosis</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes therapy</subject><subject>Diagnosis</subject><subject>DNA</subject><subject>Enzymes</subject><subject>Fasting</subject><subject>Fat mass-and obesity associated (FTO)</subject><subject>Gene polymorphism</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic diversity</subject><subject>Genetic polymorphisms</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic research</subject><subject>Genomes</subject><subject>Genotyping</subject><subject>Glucose</subject><subject>GPI-Linked Proteins - genetics</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hypertension</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Insulin Resistance - physiology</subject><subject>Iran</subject><subject>Laboratories</subject><subject>Lectins - genetics</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Obesity</subject><subject>Omentin</subject><subject>Overweight</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Polymorphism, Restriction Fragment Length - genetics</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Population</subject><subject>Restriction fragment length polymorphism</subject><subject>Studies</subject><subject>Type 2 diabetes</subject><subject>Young Adult</subject><issn>1476-511X</issn><issn>1476-511X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk9rFDEcHUSxtfoBvEjAi5ep-TeTyUVYitWFwl4qeAuZ5JfdLDPJmsy07Efx25rtrqUVySHh5b0Xfi-vqt4TfElI137OhErOa0xkTXDX1M2L6pxw0dYNIT9fPjmfVW9y3mJMsWjb19UZIxRjQdl59XuRczReTz4GFB1ajRAmH1DKlAousUA6WHR9uyqIlEy2WKI1BEC7OOzHmHYbn8eM7v20QT7keThoIfs86WCgQGiZdPA6lKP1d97OejjRA9wPe2S9XoeYwaJpvwNED0APE-S31StXuPDutF9UP66_3l59r29W35ZXi5vaNC2eamc7gSlhYLV1mgjBoem1k8A7qmXfm8b2hDjSG2eBQC-A2BJeD5pbTAxjF9Xy6Guj3qpd8qNOexW1Vw9ATGul0-TNAAo7K2xnNaa940ZLqbG0lhlpTOOMkMXry9FrN_cjWFOyTHp4Zvr8JviNWsc71TYCd6wtBp9OBin-miFPavTZwDDoAHHOitIGt5yJjhfqx3-o2zinUKIqLM6Y4O2D4Ym11mUAH1ws75qDqVo05XtbhgkurMv_sMqyMHoTAzhf8GcCchSYFHNO4B5nJFgduqmO3VSlm-rQTdUUzYen4Twq_paR_QEeQuEc</recordid><startdate>20190614</startdate><enddate>20190614</enddate><creator>Khoshi, Amirhosein</creator><creator>Bajestani, Mehdi Kaffash</creator><creator>Shakeri, Habibesadat</creator><creator>Goodarzi, Golnaz</creator><creator>Azizi, Fatemeh</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>7X7</scope><scope>7XB</scope><scope>88E</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>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-9520-1857</orcidid></search><sort><creationdate>20190614</creationdate><title>Association of Omentin rs2274907 and FTO rs9939609 gene polymorphisms with insulin resistance in Iranian individuals with newly diagnosed type 2 diabetes</title><author>Khoshi, Amirhosein ; Bajestani, Mehdi Kaffash ; Shakeri, Habibesadat ; Goodarzi, Golnaz ; Azizi, Fatemeh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-fd870213edadfa1774e5baf9e482a9bbc5db11f1bcfde1eb7e1d118bea4d01c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adipose tissue</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alpha-Ketoglutarate-Dependent Dioxygenase FTO</topic><topic>Blood glucose</topic><topic>Blood Glucose - metabolism</topic><topic>Body Mass Index</topic><topic>Body weight</topic><topic>Cardiovascular disease</topic><topic>Case-Control Studies</topic><topic>Cholesterol</topic><topic>Cytokines - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - diagnosis</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes therapy</topic><topic>Diagnosis</topic><topic>DNA</topic><topic>Enzymes</topic><topic>Fasting</topic><topic>Fat mass-and obesity associated (FTO)</topic><topic>Gene polymorphism</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic diversity</topic><topic>Genetic polymorphisms</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genetic research</topic><topic>Genomes</topic><topic>Genotyping</topic><topic>Glucose</topic><topic>GPI-Linked Proteins - genetics</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hypertension</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Insulin Resistance - physiology</topic><topic>Iran</topic><topic>Laboratories</topic><topic>Lectins - genetics</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Obesity</topic><topic>Omentin</topic><topic>Overweight</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism</topic><topic>Polymorphism, Restriction Fragment Length - genetics</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Population</topic><topic>Restriction fragment length polymorphism</topic><topic>Studies</topic><topic>Type 2 diabetes</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khoshi, Amirhosein</creatorcontrib><creatorcontrib>Bajestani, Mehdi Kaffash</creatorcontrib><creatorcontrib>Shakeri, Habibesadat</creatorcontrib><creatorcontrib>Goodarzi, Golnaz</creatorcontrib><creatorcontrib>Azizi, Fatemeh</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</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>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</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>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content (ProQuest)</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Lipids in health and disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khoshi, Amirhosein</au><au>Bajestani, Mehdi Kaffash</au><au>Shakeri, Habibesadat</au><au>Goodarzi, Golnaz</au><au>Azizi, Fatemeh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of Omentin rs2274907 and FTO rs9939609 gene polymorphisms with insulin resistance in Iranian individuals with newly diagnosed type 2 diabetes</atitle><jtitle>Lipids in health and disease</jtitle><addtitle>Lipids Health Dis</addtitle><date>2019-06-14</date><risdate>2019</risdate><volume>18</volume><issue>1</issue><spage>142</spage><epage>142</epage><pages>142-142</pages><artnum>142</artnum><issn>1476-511X</issn><eissn>1476-511X</eissn><abstract>Insulin resistance (IR) and fat accumulation in visceral adipose tissue are key players in developing type 2 diabetes (T2D). Several adipose tissue derived-gene polymorphisms are related to higher body mass index (BMI), insulin resistance and T2D. The association of omentin rs2274907 (Val109Asp) and fat-mass and obesity-associated (FTO) rs9939609 gene polymorphisms with overweight/obesity and T2D is controversial. The aim of this study was to determine the association between omentin Val109Asp and FTO rs9939609 polymorphisms and insulin resistance in newly-diagnosed T2D patients.
The case-control study included 83 newly-diagnosed T2D patients and 85 healthy matched controls, aged 20-80 years. Fasting blood glucose and insulin levels were measured by the enzymatic method and enzyme-linked-immunosorbent assay, respectively. Insulin resistance was calculated using the homeostasis model assessment (HOMA) index. Genotyping was examined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).
There are significant differences between both omentin Val109Asp and FTO rs9939609 polymorphisms and studied individuals (P = 0.011 and P = 0.0001, respectively). Both genetic polymorphisms of omentin Val109Asp and FTO rs9939609 (T/A) are significantly related to higher HOMA index (P = 0.030 and P = 0.046, respectively). However, omentin Val109Asp polymorphism was only related to individuals who were overweight/obese. Additionally, both omentin Val109Asp and FTO rs9939609 polymorphisms were significantly positively correlated to familial history of diabetes (P = 0.046 and P = 0.024, respectively).
Omentin V109D and FTO rs9939609 genetic variations may change insulin metabolism and have key roles in developing T2D through insulin resistance. Thus, the evaluation of these polymorphic regions may be helpful for predicting type 2 diabetes.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>31200723</pmid><doi>10.1186/s12944-019-1085-5</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-9520-1857</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adipose tissue Adult Aged Aged, 80 and over Alpha-Ketoglutarate-Dependent Dioxygenase FTO Blood glucose Blood Glucose - metabolism Body Mass Index Body weight Cardiovascular disease Case-Control Studies Cholesterol Cytokines - genetics Deoxyribonucleic acid Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - diagnosis Diabetes Mellitus, Type 2 - genetics Diabetes therapy Diagnosis DNA Enzymes Fasting Fat mass-and obesity associated (FTO) Gene polymorphism Genes Genetic aspects Genetic diversity Genetic polymorphisms Genetic Predisposition to Disease - genetics Genetic research Genomes Genotyping Glucose GPI-Linked Proteins - genetics Homeostasis Humans Hyperglycemia Hypertension Insulin Insulin resistance Insulin Resistance - genetics Insulin Resistance - physiology Iran Laboratories Lectins - genetics Metabolism Middle Aged Obesity Omentin Overweight Polymerase chain reaction Polymorphism Polymorphism, Restriction Fragment Length - genetics Polymorphism, Single Nucleotide - genetics Population Restriction fragment length polymorphism Studies Type 2 diabetes Young Adult |
title | Association of Omentin rs2274907 and FTO rs9939609 gene polymorphisms with insulin resistance in Iranian individuals with newly diagnosed type 2 diabetes |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T04%3A19%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Association%20of%20Omentin%20rs2274907%20and%20FTO%20rs9939609%20gene%20polymorphisms%20with%20insulin%20resistance%20in%20Iranian%20individuals%20with%20newly%20diagnosed%20type%202%20diabetes&rft.jtitle=Lipids%20in%20health%20and%20disease&rft.au=Khoshi,%20Amirhosein&rft.date=2019-06-14&rft.volume=18&rft.issue=1&rft.spage=142&rft.epage=142&rft.pages=142-142&rft.artnum=142&rft.issn=1476-511X&rft.eissn=1476-511X&rft_id=info:doi/10.1186/s12944-019-1085-5&rft_dat=%3Cgale_doaj_%3EA590763010%3C/gale_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c560t-fd870213edadfa1774e5baf9e482a9bbc5db11f1bcfde1eb7e1d118bea4d01c33%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2243374636&rft_id=info:pmid/31200723&rft_galeid=A590763010&rfr_iscdi=true |