Impaired early- but not late-phase insulin secretion in subjects with impaired fasting glucose
Subjects with impaired fasting glucose (IFG) are at increased risk for type 2 diabetes. We recently demonstrated that IFG subjects have increased hepatic insulin resistance with normal insulin sensitivity in skeletal muscle. In this study, we quantitated the insulin secretion rate from deconvolution...
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| Veröffentlicht in: | Acta diabetologica 2011-09, Vol.48 (3), p.209-217 |
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| creator | Kanat, Mustafa Norton, Luke Winnier, Diedre Jenkinson, Chris DeFronzo, Ralph A. Abdul-Ghani, Muhammad A. |
| description | Subjects with impaired fasting glucose (IFG) are at increased risk for type 2 diabetes. We recently demonstrated that IFG subjects have increased hepatic insulin resistance with normal insulin sensitivity in skeletal muscle. In this study, we quantitated the insulin secretion rate from deconvolution analysis of the plasma C-peptide concentration during an oral glucose tolerance test (OGTT) and compared the results in IFG subjects with those in subjects with impaired glucose tolerance (IGT) and normal glucose tolerance (NGT). One hundred and one NGT subjects, 64 subjects with isolated IGT, 24 subjects with isolated IFG, and 48 subjects with combined (IFG + IGT) glucose intolerance (CGI) received an OGTT. Plasma glucose, insulin, and C-peptide concentrations were measured before and every 15 min after glucose ingestion. Insulin secretion rate (ISR) was determined by deconvolution of plasma C-peptide concentration. Inverse of the Matsuda index of whole body insulin sensitivity was used as a measure of insulin resistance; 56 subjects also received a euglycemic hyperinsulinemic clamp. The insulin secretion/insulin resistance (disposition) index was calculated as the ratio between incremental area under the ISR curve (∆ISR[AUC]) to incremental area under the glucose curve (∆G[AUC]) factored by the severity of insulin resistance (measured by Matsuda index during OGTT or glucose disposal during insulin clamp). Compared to NGT, the insulin secretion/insulin resistance index during first 30 min of OGTT was reduced by 47, 49, and 74% in IFG, IGT, and CGI, respectively (all |
| doi_str_mv | 10.1007/s00592-011-0285-x |
| format | Article |
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P
= NS), but was profoundly reduced in subjects with IGT and CGI (0.31 ± 0.2 and 0.19 ± 0.11, respectively;
P
< 0.0001 vs. both NGT and IFG). Early-phase insulin secretion is impaired in both IFG and IGT, while the late-phase insulin secretion is impaired only in subjects with IGT.</description><identifier>ISSN: 0940-5429</identifier><identifier>EISSN: 1432-5233</identifier><identifier>DOI: 10.1007/s00592-011-0285-x</identifier><identifier>PMID: 21553243</identifier><identifier>CODEN: ACDAEZ</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Adult ; Blood Glucose - metabolism ; Blood Glucose - physiology ; Diabetes ; Fasting - blood ; Fasting - metabolism ; Fasting - physiology ; Female ; Glucose ; Glucose Clamp Technique ; Glucose Intolerance - blood ; Glucose Intolerance - metabolism ; Glucose Tolerance Test ; Humans ; Insulin ; Insulin - metabolism ; Insulin Resistance - physiology ; Insulin Secretion ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolic Networks and Pathways - physiology ; Middle Aged ; Original Article ; Prediabetic State - blood ; Prediabetic State - metabolism ; Risk factors ; Time Factors</subject><ispartof>Acta diabetologica, 2011-09, Vol.48 (3), p.209-217</ispartof><rights>Springer-Verlag 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c403t-1f2bc94a04c8b5b4029281b45bca823d51162e0d3fcfdc1af43bc9567ce749f43</citedby><cites>FETCH-LOGICAL-c403t-1f2bc94a04c8b5b4029281b45bca823d51162e0d3fcfdc1af43bc9567ce749f43</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/s00592-011-0285-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00592-011-0285-x$$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/21553243$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kanat, Mustafa</creatorcontrib><creatorcontrib>Norton, Luke</creatorcontrib><creatorcontrib>Winnier, Diedre</creatorcontrib><creatorcontrib>Jenkinson, Chris</creatorcontrib><creatorcontrib>DeFronzo, Ralph A.</creatorcontrib><creatorcontrib>Abdul-Ghani, Muhammad A.</creatorcontrib><title>Impaired early- but not late-phase insulin secretion in subjects with impaired fasting glucose</title><title>Acta diabetologica</title><addtitle>Acta Diabetol</addtitle><addtitle>Acta Diabetol</addtitle><description>Subjects with impaired fasting glucose (IFG) are at increased risk for type 2 diabetes. We recently demonstrated that IFG subjects have increased hepatic insulin resistance with normal insulin sensitivity in skeletal muscle. In this study, we quantitated the insulin secretion rate from deconvolution analysis of the plasma C-peptide concentration during an oral glucose tolerance test (OGTT) and compared the results in IFG subjects with those in subjects with impaired glucose tolerance (IGT) and normal glucose tolerance (NGT). One hundred and one NGT subjects, 64 subjects with isolated IGT, 24 subjects with isolated IFG, and 48 subjects with combined (IFG + IGT) glucose intolerance (CGI) received an OGTT. Plasma glucose, insulin, and C-peptide concentrations were measured before and every 15 min after glucose ingestion. Insulin secretion rate (ISR) was determined by deconvolution of plasma C-peptide concentration. Inverse of the Matsuda index of whole body insulin sensitivity was used as a measure of insulin resistance; 56 subjects also received a euglycemic hyperinsulinemic clamp. The insulin secretion/insulin resistance (disposition) index was calculated as the ratio between incremental area under the ISR curve (∆ISR[AUC]) to incremental area under the glucose curve (∆G[AUC]) factored by the severity of insulin resistance (measured by Matsuda index during OGTT or glucose disposal during insulin clamp). Compared to NGT, the insulin secretion/insulin resistance index during first 30 min of OGTT was reduced by 47, 49, and 74% in IFG, IGT, and CGI, respectively (all < 0.0001). The insulin secretion/insulin resistance index during the second hour (60–120 min) of the OGTT in subjects with IFG was similar to that in NGT (0.79 ± 0.6 vs. 0.72 ± 0.5, respectively,
P
= NS), but was profoundly reduced in subjects with IGT and CGI (0.31 ± 0.2 and 0.19 ± 0.11, respectively;
P
< 0.0001 vs. both NGT and IFG). Early-phase insulin secretion is impaired in both IFG and IGT, while the late-phase insulin secretion is impaired only in subjects with IGT.</description><subject>Adult</subject><subject>Blood Glucose - metabolism</subject><subject>Blood Glucose - physiology</subject><subject>Diabetes</subject><subject>Fasting - blood</subject><subject>Fasting - metabolism</subject><subject>Fasting - physiology</subject><subject>Female</subject><subject>Glucose</subject><subject>Glucose Clamp Technique</subject><subject>Glucose Intolerance - blood</subject><subject>Glucose Intolerance - metabolism</subject><subject>Glucose Tolerance Test</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance - physiology</subject><subject>Insulin Secretion</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolic Networks and Pathways - physiology</subject><subject>Middle Aged</subject><subject>Original Article</subject><subject>Prediabetic State - blood</subject><subject>Prediabetic State - metabolism</subject><subject>Risk factors</subject><subject>Time Factors</subject><issn>0940-5429</issn><issn>1432-5233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kU1P3DAQhi1UVJaPH8ClsnqBi-n4a-McK0QLEhIXuNZynMniVTbZ2o6Af19HC0WqVE7WyM88M_ZLyCmHCw5QfUsAuhYMOGcgjGbPe2TBlRRMCyk_kQXUCphWoj4ghymtAbiopPlMDgTXWgolF-TXzWbrQsSWoov9C6PNlOkwZtq7jGz76BLSMKSpDwNN6CPmMA50LqZmjT4n-hTyIw1vls6lHIYVXfWTHxMek_3O9QlPXs8j8vDj6v7ymt3e_by5_H7LvAKZGe9E42vlQHnT6EaBqIXhjdKNd0bIVnO-FAit7HzXeu46JQuvl5XHStWlOiJnO-82jr8nTNluQvLY927AcUrWGK2XUi9FIc8_JHllyu-BNqagX_9B1-MUh_KO2VcWBDlP5jvIxzGliJ3dxrBx8cVysHNKdpeSLSnZOSX7XHq-vIqnZoPt3463WAogdkAqV8MK4_vk_1v_AI27nVc</recordid><startdate>20110901</startdate><enddate>20110901</enddate><creator>Kanat, Mustafa</creator><creator>Norton, Luke</creator><creator>Winnier, Diedre</creator><creator>Jenkinson, Chris</creator><creator>DeFronzo, Ralph A.</creator><creator>Abdul-Ghani, Muhammad A.</creator><general>Springer Milan</general><general>Springer Nature B.V</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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20110901</creationdate><title>Impaired early- but not late-phase insulin secretion in subjects with impaired fasting glucose</title><author>Kanat, Mustafa ; 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We recently demonstrated that IFG subjects have increased hepatic insulin resistance with normal insulin sensitivity in skeletal muscle. In this study, we quantitated the insulin secretion rate from deconvolution analysis of the plasma C-peptide concentration during an oral glucose tolerance test (OGTT) and compared the results in IFG subjects with those in subjects with impaired glucose tolerance (IGT) and normal glucose tolerance (NGT). One hundred and one NGT subjects, 64 subjects with isolated IGT, 24 subjects with isolated IFG, and 48 subjects with combined (IFG + IGT) glucose intolerance (CGI) received an OGTT. Plasma glucose, insulin, and C-peptide concentrations were measured before and every 15 min after glucose ingestion. Insulin secretion rate (ISR) was determined by deconvolution of plasma C-peptide concentration. Inverse of the Matsuda index of whole body insulin sensitivity was used as a measure of insulin resistance; 56 subjects also received a euglycemic hyperinsulinemic clamp. The insulin secretion/insulin resistance (disposition) index was calculated as the ratio between incremental area under the ISR curve (∆ISR[AUC]) to incremental area under the glucose curve (∆G[AUC]) factored by the severity of insulin resistance (measured by Matsuda index during OGTT or glucose disposal during insulin clamp). Compared to NGT, the insulin secretion/insulin resistance index during first 30 min of OGTT was reduced by 47, 49, and 74% in IFG, IGT, and CGI, respectively (all < 0.0001). The insulin secretion/insulin resistance index during the second hour (60–120 min) of the OGTT in subjects with IFG was similar to that in NGT (0.79 ± 0.6 vs. 0.72 ± 0.5, respectively,
P
= NS), but was profoundly reduced in subjects with IGT and CGI (0.31 ± 0.2 and 0.19 ± 0.11, respectively;
P
< 0.0001 vs. both NGT and IFG). Early-phase insulin secretion is impaired in both IFG and IGT, while the late-phase insulin secretion is impaired only in subjects with IGT.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>21553243</pmid><doi>10.1007/s00592-011-0285-x</doi><tpages>9</tpages></addata></record> |
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| subjects | Adult Blood Glucose - metabolism Blood Glucose - physiology Diabetes Fasting - blood Fasting - metabolism Fasting - physiology Female Glucose Glucose Clamp Technique Glucose Intolerance - blood Glucose Intolerance - metabolism Glucose Tolerance Test Humans Insulin Insulin - metabolism Insulin Resistance - physiology Insulin Secretion Internal Medicine Male Medicine Medicine & Public Health Metabolic Diseases Metabolic Networks and Pathways - physiology Middle Aged Original Article Prediabetic State - blood Prediabetic State - metabolism Risk factors Time Factors |
| title | Impaired early- but not late-phase insulin secretion in subjects with impaired fasting glucose |
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