frequency of factor V Leiden mutation, ACE gene polymorphism, serum ACE activity and response to ACE inhibitor and angiotensin II receptor antagonist drugs in Iranians type II diabetic patients with microalbuminuria
The aim of present study was to determine if factor V Leiden (FVL) mutation and angiotensin converting enzyme insertion/deletion (ACE I/D) polymorphism are associated with diabetic nephropathy (DN) among Kurdish population from Western Iran. This case-control study comprised 144 unrelated adult type...
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| Veröffentlicht in: | Molecular biology reports 2011-03, Vol.38 (3), p.2117-2123 |
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| creator | Rahimi, Zohreh Felehgari, Vahid Rahimi, Mehrali Mozafari, Hadi Yari, Kheirollah Vaisi-Raygani, Asad Rezaei, Mansour Malek-Khosravi, Shohreh Khazaie, Habibolah |
| description | The aim of present study was to determine if factor V Leiden (FVL) mutation and angiotensin converting enzyme insertion/deletion (ACE I/D) polymorphism are associated with diabetic nephropathy (DN) among Kurdish population from Western Iran. This case-control study comprised 144 unrelated adult type 2 diabetic mellitus patients (T2DM) including 72 patients with microalbuminuria and 72 age and sex matched patients without nephropathy. The ACE I/D polymorphism and FVL mutation were detected by polymerase chain reaction (PCR) and PCR-RFLP, respectively. The frequency of FVL G1691A and ACE D allele in T2DM patients with microalbuminuria were 1.6 and 57%, respectively and in normoalbuminuric T2DM patients were 4.9 and 58.3%, respectively (P > 0.05). ACE genotypes affected on serum ACE activity and a better response to ACE inhibitor therapy (captopril) compared to angiotensin II receptor antagonist (losartan) was obtained with significant reduction of ACE activity in diabetic patients without nephropathy carrying DD genotype. However, the beneficial effect of losartan therapy was observed in microalbuminuric patients with II genotype compared to ID and DD genotypes. |
| doi_str_mv | 10.1007/s11033-010-0338-1 |
| format | Article |
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This case-control study comprised 144 unrelated adult type 2 diabetic mellitus patients (T2DM) including 72 patients with microalbuminuria and 72 age and sex matched patients without nephropathy. The ACE I/D polymorphism and FVL mutation were detected by polymerase chain reaction (PCR) and PCR-RFLP, respectively. The frequency of FVL G1691A and ACE D allele in T2DM patients with microalbuminuria were 1.6 and 57%, respectively and in normoalbuminuric T2DM patients were 4.9 and 58.3%, respectively (P > 0.05). ACE genotypes affected on serum ACE activity and a better response to ACE inhibitor therapy (captopril) compared to angiotensin II receptor antagonist (losartan) was obtained with significant reduction of ACE activity in diabetic patients without nephropathy carrying DD genotype. However, the beneficial effect of losartan therapy was observed in microalbuminuric patients with II genotype compared to ID and DD genotypes.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-010-0338-1</identifier><identifier>PMID: 20853144</identifier><language>eng</language><publisher>Dordrecht: Dordrecht : Springer Netherlands</publisher><subject>ACE genotypes and activity ; ACE inhibitors ; ACE protein ; Albuminuria - complications ; Albuminuria - genetics ; Alleles ; Angiotensin II receptor antagonists ; Angiotensin II receptors ; Angiotensin Receptor Antagonists - therapeutic use ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Animal Anatomy ; Animal Biochemistry ; Antagonist drugs ; Biomedical and Life Sciences ; Captopril - therapeutic use ; Coagulation factors ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - enzymology ; Diabetes Mellitus, Type 2 - genetics ; Diabetic Nephropathies - complications ; Diabetic Nephropathies - drug therapy ; Diabetic Nephropathies - enzymology ; Diabetic Nephropathies - genetics ; Drugs ; Factor V ; Factor V - genetics ; Female ; FVL ; Gene deletion ; Gene polymorphism ; Genetic Predisposition to Disease ; Histology ; Humans ; Insertion ; Iran ; Life Sciences ; Losartan - therapeutic use ; Male ; Microalbuminuria ; Middle Aged ; Molecular biology ; Morphology ; Mutation ; Nephropathy ; Peptidyl-dipeptidase A ; Peptidyl-Dipeptidase A - blood ; Peptidyl-Dipeptidase A - genetics ; Polymerase chain reaction ; Polymorphism ; Polymorphism, Genetic ; Restriction fragment length polymorphism ; Sex ; Treatment Outcome ; Type 2 diabetes mellitus</subject><ispartof>Molecular biology reports, 2011-03, Vol.38 (3), p.2117-2123</ispartof><rights>Springer Science+Business Media B.V. 2010</rights><rights>Springer Science+Business Media B.V. 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-71da85b777e378987e5e70f71f6b827e994d133911fcb8ccc3cf363fde6e3ff63</citedby><cites>FETCH-LOGICAL-c426t-71da85b777e378987e5e70f71f6b827e994d133911fcb8ccc3cf363fde6e3ff63</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/s11033-010-0338-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-010-0338-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20853144$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rahimi, Zohreh</creatorcontrib><creatorcontrib>Felehgari, Vahid</creatorcontrib><creatorcontrib>Rahimi, Mehrali</creatorcontrib><creatorcontrib>Mozafari, Hadi</creatorcontrib><creatorcontrib>Yari, Kheirollah</creatorcontrib><creatorcontrib>Vaisi-Raygani, Asad</creatorcontrib><creatorcontrib>Rezaei, Mansour</creatorcontrib><creatorcontrib>Malek-Khosravi, Shohreh</creatorcontrib><creatorcontrib>Khazaie, Habibolah</creatorcontrib><title>frequency of factor V Leiden mutation, ACE gene polymorphism, serum ACE activity and response to ACE inhibitor and angiotensin II receptor antagonist drugs in Iranians type II diabetic patients with microalbuminuria</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>The aim of present study was to determine if factor V Leiden (FVL) mutation and angiotensin converting enzyme insertion/deletion (ACE I/D) polymorphism are associated with diabetic nephropathy (DN) among Kurdish population from Western Iran. This case-control study comprised 144 unrelated adult type 2 diabetic mellitus patients (T2DM) including 72 patients with microalbuminuria and 72 age and sex matched patients without nephropathy. The ACE I/D polymorphism and FVL mutation were detected by polymerase chain reaction (PCR) and PCR-RFLP, respectively. The frequency of FVL G1691A and ACE D allele in T2DM patients with microalbuminuria were 1.6 and 57%, respectively and in normoalbuminuric T2DM patients were 4.9 and 58.3%, respectively (P > 0.05). ACE genotypes affected on serum ACE activity and a better response to ACE inhibitor therapy (captopril) compared to angiotensin II receptor antagonist (losartan) was obtained with significant reduction of ACE activity in diabetic patients without nephropathy carrying DD genotype. However, the beneficial effect of losartan therapy was observed in microalbuminuric patients with II genotype compared to ID and DD genotypes.</description><subject>ACE genotypes and activity</subject><subject>ACE inhibitors</subject><subject>ACE protein</subject><subject>Albuminuria - complications</subject><subject>Albuminuria - genetics</subject><subject>Alleles</subject><subject>Angiotensin II receptor antagonists</subject><subject>Angiotensin II receptors</subject><subject>Angiotensin Receptor Antagonists - therapeutic use</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Antagonist drugs</subject><subject>Biomedical and Life Sciences</subject><subject>Captopril - therapeutic use</subject><subject>Coagulation factors</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - enzymology</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetic Nephropathies - complications</subject><subject>Diabetic Nephropathies - drug therapy</subject><subject>Diabetic Nephropathies - enzymology</subject><subject>Diabetic Nephropathies - genetics</subject><subject>Drugs</subject><subject>Factor V</subject><subject>Factor V - genetics</subject><subject>Female</subject><subject>FVL</subject><subject>Gene deletion</subject><subject>Gene polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>Histology</subject><subject>Humans</subject><subject>Insertion</subject><subject>Iran</subject><subject>Life Sciences</subject><subject>Losartan - therapeutic use</subject><subject>Male</subject><subject>Microalbuminuria</subject><subject>Middle Aged</subject><subject>Molecular biology</subject><subject>Morphology</subject><subject>Mutation</subject><subject>Nephropathy</subject><subject>Peptidyl-dipeptidase A</subject><subject>Peptidyl-Dipeptidase A - blood</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Restriction fragment length polymorphism</subject><subject>Sex</subject><subject>Treatment Outcome</subject><subject>Type 2 diabetes mellitus</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkkFv1DAQhSMEokvhB3ABiwuXBjxxEjvHatXCSitxgHKNHGecdbWxg-2A9pfyd-o0BSQOcJrD-96zZ_Sy7CXQd0Apfx8AKGM5BZqnKXJ4lG2g4iwvGy4eZxvKKOSlqOAsexbCLaW0BF49zc4KKioGZbnJfmqP32a06kScJlqq6Dz5SvZoerRknKOMxtkLcrm9IgNaJJM7nkbnp4MJ4wUJ6OfxXkxO893EE5G2Jx7D5GxAEt29aOzBdGaJXlRpB-Mi2mAs2e0SrHBatSgHZ02IpPfzEMiie2mNtIHE04QL3RvZYTSKTOlnaGMgP0w8kNEo7-Sxm0djZ2_k8-yJlseALx7meXZzffVl-zHff_qw217uc1UWdcw59FJUHeccGReN4Fghp5qDrjtRcGyasgfGGgCtOqGUYkqzmukea2Ra1-w8e7vmTt6lO4bYjiYoPB6lRTeHVtSUNayoxP_JsqFQFPVCvvmLvHWzt2mNBIm6KUE0CYIVSnuH4FG3kzej9KcWaLu0o13b0aZ2tEs7WkieVw_Bczdi_9vxqw4JKFYgJMkO6P-8_K_U16tJS9fKwZvQ3nwuKKTyNUxUlLM7YwDReA</recordid><startdate>20110301</startdate><enddate>20110301</enddate><creator>Rahimi, Zohreh</creator><creator>Felehgari, Vahid</creator><creator>Rahimi, Mehrali</creator><creator>Mozafari, Hadi</creator><creator>Yari, Kheirollah</creator><creator>Vaisi-Raygani, Asad</creator><creator>Rezaei, Mansour</creator><creator>Malek-Khosravi, Shohreh</creator><creator>Khazaie, Habibolah</creator><general>Dordrecht : Springer Netherlands</general><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>FBQ</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>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20110301</creationdate><title>frequency of factor V Leiden mutation, ACE gene polymorphism, serum ACE activity and response to ACE inhibitor and angiotensin II receptor antagonist drugs in Iranians type II diabetic patients with microalbuminuria</title><author>Rahimi, Zohreh ; Felehgari, Vahid ; Rahimi, Mehrali ; Mozafari, Hadi ; Yari, Kheirollah ; Vaisi-Raygani, Asad ; Rezaei, Mansour ; Malek-Khosravi, Shohreh ; Khazaie, Habibolah</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-71da85b777e378987e5e70f71f6b827e994d133911fcb8ccc3cf363fde6e3ff63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>ACE genotypes and activity</topic><topic>ACE inhibitors</topic><topic>ACE protein</topic><topic>Albuminuria - 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genetics</topic><topic>Female</topic><topic>FVL</topic><topic>Gene deletion</topic><topic>Gene polymorphism</topic><topic>Genetic Predisposition to Disease</topic><topic>Histology</topic><topic>Humans</topic><topic>Insertion</topic><topic>Iran</topic><topic>Life Sciences</topic><topic>Losartan - therapeutic use</topic><topic>Male</topic><topic>Microalbuminuria</topic><topic>Middle Aged</topic><topic>Molecular biology</topic><topic>Morphology</topic><topic>Mutation</topic><topic>Nephropathy</topic><topic>Peptidyl-dipeptidase A</topic><topic>Peptidyl-Dipeptidase A - blood</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Restriction fragment length polymorphism</topic><topic>Sex</topic><topic>Treatment Outcome</topic><topic>Type 2 diabetes mellitus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rahimi, Zohreh</creatorcontrib><creatorcontrib>Felehgari, Vahid</creatorcontrib><creatorcontrib>Rahimi, Mehrali</creatorcontrib><creatorcontrib>Mozafari, Hadi</creatorcontrib><creatorcontrib>Yari, Kheirollah</creatorcontrib><creatorcontrib>Vaisi-Raygani, Asad</creatorcontrib><creatorcontrib>Rezaei, Mansour</creatorcontrib><creatorcontrib>Malek-Khosravi, Shohreh</creatorcontrib><creatorcontrib>Khazaie, Habibolah</creatorcontrib><collection>AGRIS</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>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rahimi, Zohreh</au><au>Felehgari, Vahid</au><au>Rahimi, Mehrali</au><au>Mozafari, Hadi</au><au>Yari, Kheirollah</au><au>Vaisi-Raygani, Asad</au><au>Rezaei, Mansour</au><au>Malek-Khosravi, Shohreh</au><au>Khazaie, Habibolah</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>frequency of factor V Leiden mutation, ACE gene polymorphism, serum ACE activity and response to ACE inhibitor and angiotensin II receptor antagonist drugs in Iranians type II diabetic patients with microalbuminuria</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2011-03-01</date><risdate>2011</risdate><volume>38</volume><issue>3</issue><spage>2117</spage><epage>2123</epage><pages>2117-2123</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>The aim of present study was to determine if factor V Leiden (FVL) mutation and angiotensin converting enzyme insertion/deletion (ACE I/D) polymorphism are associated with diabetic nephropathy (DN) among Kurdish population from Western Iran. This case-control study comprised 144 unrelated adult type 2 diabetic mellitus patients (T2DM) including 72 patients with microalbuminuria and 72 age and sex matched patients without nephropathy. The ACE I/D polymorphism and FVL mutation were detected by polymerase chain reaction (PCR) and PCR-RFLP, respectively. The frequency of FVL G1691A and ACE D allele in T2DM patients with microalbuminuria were 1.6 and 57%, respectively and in normoalbuminuric T2DM patients were 4.9 and 58.3%, respectively (P > 0.05). ACE genotypes affected on serum ACE activity and a better response to ACE inhibitor therapy (captopril) compared to angiotensin II receptor antagonist (losartan) was obtained with significant reduction of ACE activity in diabetic patients without nephropathy carrying DD genotype. However, the beneficial effect of losartan therapy was observed in microalbuminuric patients with II genotype compared to ID and DD genotypes.</abstract><cop>Dordrecht</cop><pub>Dordrecht : Springer Netherlands</pub><pmid>20853144</pmid><doi>10.1007/s11033-010-0338-1</doi><tpages>7</tpages></addata></record> |
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| issn | 0301-4851 1573-4978 |
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| subjects | ACE genotypes and activity ACE inhibitors ACE protein Albuminuria - complications Albuminuria - genetics Alleles Angiotensin II receptor antagonists Angiotensin II receptors Angiotensin Receptor Antagonists - therapeutic use Angiotensin-Converting Enzyme Inhibitors - therapeutic use Animal Anatomy Animal Biochemistry Antagonist drugs Biomedical and Life Sciences Captopril - therapeutic use Coagulation factors Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - enzymology Diabetes Mellitus, Type 2 - genetics Diabetic Nephropathies - complications Diabetic Nephropathies - drug therapy Diabetic Nephropathies - enzymology Diabetic Nephropathies - genetics Drugs Factor V Factor V - genetics Female FVL Gene deletion Gene polymorphism Genetic Predisposition to Disease Histology Humans Insertion Iran Life Sciences Losartan - therapeutic use Male Microalbuminuria Middle Aged Molecular biology Morphology Mutation Nephropathy Peptidyl-dipeptidase A Peptidyl-Dipeptidase A - blood Peptidyl-Dipeptidase A - genetics Polymerase chain reaction Polymorphism Polymorphism, Genetic Restriction fragment length polymorphism Sex Treatment Outcome Type 2 diabetes mellitus |
| title | frequency of factor V Leiden mutation, ACE gene polymorphism, serum ACE activity and response to ACE inhibitor and angiotensin II receptor antagonist drugs in Iranians type II diabetic patients with microalbuminuria |
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