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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Veröffentlicht in:Journal of inherited metabolic disease 2000-11, Vol.23 (7), p.705-712
Hauptverfasser: Krugluger, W., Festa, A., Shnawa, N., Bucher, J., Boltz‐Nitulescu, G., Schernthaner, G., Hopmeier, P.
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container_issue 7
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container_title Journal of inherited metabolic disease
container_volume 23
creator Krugluger, W.
Festa, A.
Shnawa, N.
Bucher, J.
Boltz‐Nitulescu, G.
Schernthaner, G.
Hopmeier, P.
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
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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&lt;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&lt;0.0001) and T/G genotype (r=0.24, p&lt;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&amp;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&lt;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&lt;0.0001) and T/G genotype (r=0.24, p&lt;0.03) but not in PW with G/G genotype (r=0.01, p=0.9). 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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 &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health &amp; 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 &amp; Medical Complete (Alumni)</collection><collection>Health &amp; 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&lt;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&lt;0.0001) and T/G genotype (r=0.24, p&lt;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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