A serine/alanine polymorphism in the nucleotide‐binding fold‐2 of the sulphonylurea receptor‐1 (S1369A) is associated with enhanced glucose‐induced insulin secretion during pregnancy
The sulphonylurea receptor‐1 (SUR‐1) regulates glucose‐induced insulin secretion by controlling K+‐ATP channel activity of the pancreatic β‐cell membrane. In this study, we investigated the putative role of a T/G‐polymorphism (exon 33, codon 1369; S1369A) in the adenosine diphosphate‐sensing nucleot...
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description | The sulphonylurea receptor‐1 (SUR‐1) regulates glucose‐induced insulin secretion by controlling K+‐ATP channel activity of the pancreatic β‐cell membrane. In this study, we investigated the putative role of a T/G‐polymorphism (exon 33, codon 1369; S1369A) in the adenosine diphosphate‐sensing nucleotide‐binding fold‐2 (NBF‐2) of the SUR‐1 on glucose‐induced insulin secretion during an oral glucose tolerance test in pregnant women (PW; n=182). Compared to PW with the T/T genotype, statistically significant elevated C‐peptide concentrations were found 60 min after glucose intake in PW with the T/G and G/G genotype (T/T 9.0±0.4 ng/ml vs T/G 10.8±0.4 ng/ml or G/G 10.8±0.7 ng/ml, p=0.01). Furthermore, compared to PW with T/T genotype the ΔC‐peptide (60/0 min) was significantly enhanced in PW with T/G or G/G genotype (T/T 6.7±0.3 vs T/G 8.9±0.4 or G/G 8.9±0.7, p=0.0009). A significant correlation of C‐peptide concentrations with blood glucose (BG) 60 min after glucose intake was only found in PW with the T/T genotype (r=0.6, p |
doi_str_mv | 10.1023/A:1005630912875 |
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In this study, we investigated the putative role of a T/G‐polymorphism (exon 33, codon 1369; S1369A) in the adenosine diphosphate‐sensing nucleotide‐binding fold‐2 (NBF‐2) of the SUR‐1 on glucose‐induced insulin secretion during an oral glucose tolerance test in pregnant women (PW; n=182). Compared to PW with the T/T genotype, statistically significant elevated C‐peptide concentrations were found 60 min after glucose intake in PW with the T/G and G/G genotype (T/T 9.0±0.4 ng/ml vs T/G 10.8±0.4 ng/ml or G/G 10.8±0.7 ng/ml, p=0.01). Furthermore, compared to PW with T/T genotype the ΔC‐peptide (60/0 min) was significantly enhanced in PW with T/G or G/G genotype (T/T 6.7±0.3 vs T/G 8.9±0.4 or G/G 8.9±0.7, p=0.0009). A significant correlation of C‐peptide concentrations with blood glucose (BG) 60 min after glucose intake was only found in PW with the T/T genotype (r=0.6, p<0.0004). Similarly, a significant correlation of insulin concentrations with BG 60 min after glucose intake was observed in PW with T/T genotype (r=0.5, p<0.0001) and T/G genotype (r=0.24, p<0.03) but not in PW with G/G genotype (r=0.01, p=0.9). From our data we conclude that in PW with the alanine substitution in the NBF‐2 region, the insulin response of the pancreatic β‐cell after glucose intake is enhanced and does not correlate with actual BG levels</description><identifier>ISSN: 0141-8955</identifier><identifier>EISSN: 1573-2665</identifier><identifier>DOI: 10.1023/A:1005630912875</identifier><identifier>PMID: 11117432</identifier><identifier>CODEN: JIMDDP</identifier><language>eng</language><publisher>Dordrecht: Kluwer Academic Publishers</publisher><subject>Alanine - genetics ; Alanine - metabolism ; ATP-Binding Cassette Transporters ; Binding Sites ; Biological and medical sciences ; Blood Glucose - analysis ; C-Peptide - blood ; Codon ; Diabetes, Gestational - blood ; Diabetes, Gestational - genetics ; Endocrine pancreas ; Exons ; Female ; Fundamental and applied biological sciences. Psychology ; Genetic Variation ; Glucose - metabolism ; Glucose - pharmacology ; Hormones. Régulation ; Humans ; Insulin - blood ; Insulin - metabolism ; Insulin Secretion ; Polymorphism, Genetic ; Potassium Channels - genetics ; Potassium Channels - metabolism ; Potassium Channels, Inwardly Rectifying ; Pregnancy ; Receptors, Drug - genetics ; Receptors, Drug - metabolism ; Serine - genetics ; Serine - metabolism ; Sulfonylurea Receptors ; Vertebrates: endocrinology</subject><ispartof>Journal of inherited metabolic disease, 2000-11, Vol.23 (7), p.705-712</ispartof><rights>2000 SSIEM</rights><rights>2001 INIST-CNRS</rights><rights>Copyright Kluwer Academic Publishers Nov 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3945-ce2b8d69affb55c9db2d472d98d4eb3de979009897191fdd2b1cacb2e35cbcd93</citedby><cites>FETCH-LOGICAL-c3945-ce2b8d69affb55c9db2d472d98d4eb3de979009897191fdd2b1cacb2e35cbcd93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1023%2FA%3A1005630912875$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1023%2FA%3A1005630912875$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=805810$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11117432$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Krugluger, W.</creatorcontrib><creatorcontrib>Festa, A.</creatorcontrib><creatorcontrib>Shnawa, N.</creatorcontrib><creatorcontrib>Bucher, J.</creatorcontrib><creatorcontrib>Boltz‐Nitulescu, G.</creatorcontrib><creatorcontrib>Schernthaner, G.</creatorcontrib><creatorcontrib>Hopmeier, P.</creatorcontrib><title>A serine/alanine polymorphism in the nucleotide‐binding fold‐2 of the sulphonylurea receptor‐1 (S1369A) is associated with enhanced glucose‐induced insulin secretion during pregnancy</title><title>Journal of inherited metabolic disease</title><addtitle>J Inherit Metab Dis</addtitle><description>The sulphonylurea receptor‐1 (SUR‐1) regulates glucose‐induced insulin secretion by controlling K+‐ATP channel activity of the pancreatic β‐cell membrane. In this study, we investigated the putative role of a T/G‐polymorphism (exon 33, codon 1369; S1369A) in the adenosine diphosphate‐sensing nucleotide‐binding fold‐2 (NBF‐2) of the SUR‐1 on glucose‐induced insulin secretion during an oral glucose tolerance test in pregnant women (PW; n=182). Compared to PW with the T/T genotype, statistically significant elevated C‐peptide concentrations were found 60 min after glucose intake in PW with the T/G and G/G genotype (T/T 9.0±0.4 ng/ml vs T/G 10.8±0.4 ng/ml or G/G 10.8±0.7 ng/ml, p=0.01). Furthermore, compared to PW with T/T genotype the ΔC‐peptide (60/0 min) was significantly enhanced in PW with T/G or G/G genotype (T/T 6.7±0.3 vs T/G 8.9±0.4 or G/G 8.9±0.7, p=0.0009). A significant correlation of C‐peptide concentrations with blood glucose (BG) 60 min after glucose intake was only found in PW with the T/T genotype (r=0.6, p<0.0004). Similarly, a significant correlation of insulin concentrations with BG 60 min after glucose intake was observed in PW with T/T genotype (r=0.5, p<0.0001) and T/G genotype (r=0.24, p<0.03) but not in PW with G/G genotype (r=0.01, p=0.9). From our data we conclude that in PW with the alanine substitution in the NBF‐2 region, the insulin response of the pancreatic β‐cell after glucose intake is enhanced and does not correlate with actual BG levels</description><subject>Alanine - genetics</subject><subject>Alanine - metabolism</subject><subject>ATP-Binding Cassette Transporters</subject><subject>Binding Sites</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - analysis</subject><subject>C-Peptide - blood</subject><subject>Codon</subject><subject>Diabetes, Gestational - blood</subject><subject>Diabetes, Gestational - genetics</subject><subject>Endocrine pancreas</subject><subject>Exons</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Variation</subject><subject>Glucose - metabolism</subject><subject>Glucose - pharmacology</subject><subject>Hormones. Régulation</subject><subject>Humans</subject><subject>Insulin - blood</subject><subject>Insulin - metabolism</subject><subject>Insulin Secretion</subject><subject>Polymorphism, Genetic</subject><subject>Potassium Channels - genetics</subject><subject>Potassium Channels - metabolism</subject><subject>Potassium Channels, Inwardly Rectifying</subject><subject>Pregnancy</subject><subject>Receptors, Drug - genetics</subject><subject>Receptors, Drug - metabolism</subject><subject>Serine - genetics</subject><subject>Serine - metabolism</subject><subject>Sulfonylurea Receptors</subject><subject>Vertebrates: endocrinology</subject><issn>0141-8955</issn><issn>1573-2665</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU1uFDEQhVsIRIbAmh2yQEKwGMY_7XGbXSvhJyiIBbBuue3qGUceu2O3FfUuR-BEHIaT4GFGINjgTamsr-qV3quqxwS_IpiyVfuaYMzXDEtCG8HvVAvCBVvS9ZrfrRaY1GTZSM5PqgcpXWGMZcP5_eqElCdqRhfV9xYliNbDSjnlS0VjcPMuxHFr0w5Zj6YtIJ-1gzBZAz9uv_XWG-s3aAjOlJaiMPyCUnbjNvjZ5QgKRdAwTiEWgqAXnwlby_YlsgmplIK2agKDbuy0ReC3yuvSbVzWIe0VikDe_1hfdpYTEugIkw0emRz30mOEjS9T88Pq3qBcgkfHelp9ffvmy9n75eWndxdn7eVSM1nzpQbaN2Yt1TD0nGtpempqQY1sTA09MyCF3JsjBZFkMIb2RCvdU2Bc99pIdlo9P-wdY7jOkKZuZ5MGVzyDkFMnaN0IJkgBn_4DXoUcfbmto6RpqJS1KNDqAOkYUoowdGO0OxXnjuBun2vXdn_lWiaeHNfmfgfmD38MsgDPjoBKWrkhFnds-s01mDcEF4ofqBvrYP6favfh4uM5Fpizn4WjwT0</recordid><startdate>200011</startdate><enddate>200011</enddate><creator>Krugluger, W.</creator><creator>Festa, A.</creator><creator>Shnawa, N.</creator><creator>Bucher, J.</creator><creator>Boltz‐Nitulescu, G.</creator><creator>Schernthaner, G.</creator><creator>Hopmeier, P.</creator><general>Kluwer Academic Publishers</general><general>Springer</general><general>Blackwell Publishing Ltd</general><scope>IQODW</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200011</creationdate><title>A serine/alanine polymorphism in the nucleotide‐binding fold‐2 of the sulphonylurea receptor‐1 (S1369A) is associated with enhanced glucose‐induced insulin secretion during pregnancy</title><author>Krugluger, W. ; Festa, A. ; Shnawa, N. ; Bucher, J. ; Boltz‐Nitulescu, G. ; Schernthaner, G. ; Hopmeier, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3945-ce2b8d69affb55c9db2d472d98d4eb3de979009897191fdd2b1cacb2e35cbcd93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Alanine - genetics</topic><topic>Alanine - metabolism</topic><topic>ATP-Binding Cassette Transporters</topic><topic>Binding Sites</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - analysis</topic><topic>C-Peptide - blood</topic><topic>Codon</topic><topic>Diabetes, Gestational - blood</topic><topic>Diabetes, Gestational - genetics</topic><topic>Endocrine pancreas</topic><topic>Exons</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic Variation</topic><topic>Glucose - metabolism</topic><topic>Glucose - pharmacology</topic><topic>Hormones. Régulation</topic><topic>Humans</topic><topic>Insulin - blood</topic><topic>Insulin - metabolism</topic><topic>Insulin Secretion</topic><topic>Polymorphism, Genetic</topic><topic>Potassium Channels - genetics</topic><topic>Potassium Channels - metabolism</topic><topic>Potassium Channels, Inwardly Rectifying</topic><topic>Pregnancy</topic><topic>Receptors, Drug - genetics</topic><topic>Receptors, Drug - metabolism</topic><topic>Serine - genetics</topic><topic>Serine - metabolism</topic><topic>Sulfonylurea Receptors</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Krugluger, W.</creatorcontrib><creatorcontrib>Festa, A.</creatorcontrib><creatorcontrib>Shnawa, N.</creatorcontrib><creatorcontrib>Bucher, J.</creatorcontrib><creatorcontrib>Boltz‐Nitulescu, G.</creatorcontrib><creatorcontrib>Schernthaner, G.</creatorcontrib><creatorcontrib>Hopmeier, P.</creatorcontrib><collection>Pascal-Francis</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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 China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of inherited metabolic disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Krugluger, W.</au><au>Festa, A.</au><au>Shnawa, N.</au><au>Bucher, J.</au><au>Boltz‐Nitulescu, G.</au><au>Schernthaner, G.</au><au>Hopmeier, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A serine/alanine polymorphism in the nucleotide‐binding fold‐2 of the sulphonylurea receptor‐1 (S1369A) is associated with enhanced glucose‐induced insulin secretion during pregnancy</atitle><jtitle>Journal of inherited metabolic disease</jtitle><addtitle>J Inherit Metab Dis</addtitle><date>2000-11</date><risdate>2000</risdate><volume>23</volume><issue>7</issue><spage>705</spage><epage>712</epage><pages>705-712</pages><issn>0141-8955</issn><eissn>1573-2665</eissn><coden>JIMDDP</coden><abstract>The sulphonylurea receptor‐1 (SUR‐1) regulates glucose‐induced insulin secretion by controlling K+‐ATP channel activity of the pancreatic β‐cell membrane. In this study, we investigated the putative role of a T/G‐polymorphism (exon 33, codon 1369; S1369A) in the adenosine diphosphate‐sensing nucleotide‐binding fold‐2 (NBF‐2) of the SUR‐1 on glucose‐induced insulin secretion during an oral glucose tolerance test in pregnant women (PW; n=182). Compared to PW with the T/T genotype, statistically significant elevated C‐peptide concentrations were found 60 min after glucose intake in PW with the T/G and G/G genotype (T/T 9.0±0.4 ng/ml vs T/G 10.8±0.4 ng/ml or G/G 10.8±0.7 ng/ml, p=0.01). Furthermore, compared to PW with T/T genotype the ΔC‐peptide (60/0 min) was significantly enhanced in PW with T/G or G/G genotype (T/T 6.7±0.3 vs T/G 8.9±0.4 or G/G 8.9±0.7, p=0.0009). A significant correlation of C‐peptide concentrations with blood glucose (BG) 60 min after glucose intake was only found in PW with the T/T genotype (r=0.6, p<0.0004). Similarly, a significant correlation of insulin concentrations with BG 60 min after glucose intake was observed in PW with T/T genotype (r=0.5, p<0.0001) and T/G genotype (r=0.24, p<0.03) but not in PW with G/G genotype (r=0.01, p=0.9). From our data we conclude that in PW with the alanine substitution in the NBF‐2 region, the insulin response of the pancreatic β‐cell after glucose intake is enhanced and does not correlate with actual BG levels</abstract><cop>Dordrecht</cop><pub>Kluwer Academic Publishers</pub><pmid>11117432</pmid><doi>10.1023/A:1005630912875</doi><tpages>8</tpages></addata></record> |
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subjects | Alanine - genetics Alanine - metabolism ATP-Binding Cassette Transporters Binding Sites Biological and medical sciences Blood Glucose - analysis C-Peptide - blood Codon Diabetes, Gestational - blood Diabetes, Gestational - genetics Endocrine pancreas Exons Female Fundamental and applied biological sciences. Psychology Genetic Variation Glucose - metabolism Glucose - pharmacology Hormones. Régulation Humans Insulin - blood Insulin - metabolism Insulin Secretion Polymorphism, Genetic Potassium Channels - genetics Potassium Channels - metabolism Potassium Channels, Inwardly Rectifying Pregnancy Receptors, Drug - genetics Receptors, Drug - metabolism Serine - genetics Serine - metabolism Sulfonylurea Receptors Vertebrates: endocrinology |
title | A serine/alanine polymorphism in the nucleotide‐binding fold‐2 of the sulphonylurea receptor‐1 (S1369A) is associated with enhanced glucose‐induced insulin secretion during pregnancy |
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