Adequately adapted insulin secretion and decreased hepatic insulin extraction cause elevated insulin concentrations in insulin resistant non-diabetic adrenal incidentaloma patients

Insulin-resistance is commonly found in adrenal incidentaloma (AI) patients. However, little is known about beta-cell secretion in AI, because comparisons are difficult, since beta-cell-function varies with altered insulin-sensitivity. To retrospectively analyze beta-cell function in non-diabetic AI...

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Published in:PloS one 2013-10, Vol.8 (10), p.e77326-e77326
Main Authors: Anderwald, Christian-Heinz, Tura, Andrea, Gessl, Alois, Luger, Anton, Pacini, Giovanni, Krebs, Michael
Format: Article
Language:English
Subjects:
Adaptation
Adrenal Gland Neoplasms - metabolism
Anthropometry
Beta cells
Blood Glucose
Body measurements
C-Peptide - blood
Case-Control Studies
Comparative analysis
Control methods
Cortisol
Dexamethasone
Diabetes mellitus
Female
Glucose
Glucose tolerance
Glucose Tolerance Test
Humans
Insulin
Insulin - blood
Insulin - metabolism
Insulin Resistance
Insulin Secretion
Insulin-Secreting Cells - metabolism
Liver
Liver - metabolism
Male
Males
Mathematical analysis
Mathematical models
Middle Aged
Patients
Peptides
Retrospective Studies
Risk Factors
Rodents
Secretion
Sensitivity
Sensitivity analysis
Studies
Subgroups
Type 2 diabetes
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cited_by cdi_FETCH-LOGICAL-c692t-7aa93125ee6d3a260eaee301216ed233ccb544292951333c4521eb2e28167a203
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container_end_page e77326
container_issue 10
container_start_page e77326
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creator Anderwald, Christian-Heinz
Tura, Andrea
Gessl, Alois
Luger, Anton
Pacini, Giovanni
Krebs, Michael
description Insulin-resistance is commonly found in adrenal incidentaloma (AI) patients. However, little is known about beta-cell secretion in AI, because comparisons are difficult, since beta-cell-function varies with altered insulin-sensitivity. To retrospectively analyze beta-cell function in non-diabetic AI, compared to healthy controls (CON). AI (n=217, 34%males, 57 ± 1 years, body-mass-index:27.7 ± 0.3 kg/m(2)) and CON [n = 25, 32%males, 56 ± 1 years, 26.7 ± 0.8 kg/m(2)] with comparable anthropometry (p ≥ 0.31) underwent oral-glucose-tolerance-tests (OGTTs) with glucose, insulin, and C-peptide measurements. 1mg-dexamethasone-suppression-tests were performed in AI. AI were divided according to post-dexamethasone-suppression-test cortisol-thresholds of 1.8 and 5 µg/dL into 3 subgroups: pDexa5 µg/dL. Using mathematical modeling, whole-body insulin-sensitivity [Clamp-like-Index (CLIX)], insulinogenic Index, Disposition Index, Adaptation Index, and hepatic insulin extraction were calculated. CLIX was lower in AI combined (4.9 ± 0.2 mg · kg(-1) · min(-1)), pDexa
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However, little is known about beta-cell secretion in AI, because comparisons are difficult, since beta-cell-function varies with altered insulin-sensitivity. To retrospectively analyze beta-cell function in non-diabetic AI, compared to healthy controls (CON). AI (n=217, 34%males, 57 ± 1 years, body-mass-index:27.7 ± 0.3 kg/m(2)) and CON [n = 25, 32%males, 56 ± 1 years, 26.7 ± 0.8 kg/m(2)] with comparable anthropometry (p ≥ 0.31) underwent oral-glucose-tolerance-tests (OGTTs) with glucose, insulin, and C-peptide measurements. 1mg-dexamethasone-suppression-tests were performed in AI. AI were divided according to post-dexamethasone-suppression-test cortisol-thresholds of 1.8 and 5 µg/dL into 3 subgroups: pDexa<1.8 µg/dL, pDexa1.8-5 µg/dL and pDexa>5 µg/dL. Using mathematical modeling, whole-body insulin-sensitivity [Clamp-like-Index (CLIX)], insulinogenic Index, Disposition Index, Adaptation Index, and hepatic insulin extraction were calculated. CLIX was lower in AI combined (4.9 ± 0.2 mg · kg(-1) · min(-1)), pDexa<1.8 µg/dL (4.9 ± 0.3) and pDexa1.8-5 µg/dL (4.7 ± 0.3, p<0.04 vs.CON:6.7 ± 0.4). Insulinogenic and Disposition Indexes were 35%-97% higher in AI and each subgroup (p<0.008 vs.CON), whereas C-peptide-derived Adaptation Index, compensating for insulin-resistance, was comparable between AI, subgroups, and CON. Mathematical estimation of insulin-derived (insulinogenic and Disposition) Indexes from associations to insulin-sensitivity in CON revealed that AI-subgroups had ~19%-32% higher insulin-secretion than expectable. These insulin-secretion-index differences negatively (r=-0.45, p<0.001) correlated with hepatic insulin extraction, which was 13-16% lower in AI and subgroups (p<0.003 vs.CON). AI-patients show insulin-resistance, but adequately adapted insulin secretion with higher insulin concentrations during an OGTT, because of decreased hepatic insulin extraction; this finding affects all AI-patients, regardless of dexamethasone-suppression-test outcome.]]></description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0077326</identifier><identifier>PMID: 24146977</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptation ; Adrenal Gland Neoplasms - metabolism ; Anthropometry ; Beta cells ; Blood Glucose ; Body measurements ; C-Peptide - blood ; Case-Control Studies ; Comparative analysis ; Control methods ; Cortisol ; Dexamethasone ; Diabetes mellitus ; Female ; Glucose ; Glucose tolerance ; Glucose Tolerance Test ; Humans ; Insulin ; Insulin - blood ; Insulin - metabolism ; Insulin Resistance ; Insulin Secretion ; Insulin-Secreting Cells - metabolism ; Liver ; Liver - metabolism ; Male ; Males ; Mathematical analysis ; Mathematical models ; Middle Aged ; Patients ; Peptides ; Retrospective Studies ; Risk Factors ; Rodents ; Secretion ; Sensitivity ; Sensitivity analysis ; Studies ; Subgroups ; Type 2 diabetes</subject><ispartof>PloS one, 2013-10, Vol.8 (10), p.e77326-e77326</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Anderwald et al. 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AI-patients show insulin-resistance, but adequately adapted insulin secretion with higher insulin concentrations during an OGTT, because of decreased hepatic insulin extraction; this finding affects all AI-patients, regardless of dexamethasone-suppression-test outcome.]]></description><subject>Adaptation</subject><subject>Adrenal Gland Neoplasms - metabolism</subject><subject>Anthropometry</subject><subject>Beta cells</subject><subject>Blood Glucose</subject><subject>Body measurements</subject><subject>C-Peptide - blood</subject><subject>Case-Control Studies</subject><subject>Comparative analysis</subject><subject>Control methods</subject><subject>Cortisol</subject><subject>Dexamethasone</subject><subject>Diabetes mellitus</subject><subject>Female</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Glucose Tolerance Test</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance</subject><subject>Insulin Secretion</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Males</subject><subject>Mathematical analysis</subject><subject>Mathematical models</subject><subject>Middle Aged</subject><subject>Patients</subject><subject>Peptides</subject><subject>Retrospective Studies</subject><subject>Risk Factors</subject><subject>Rodents</subject><subject>Secretion</subject><subject>Sensitivity</subject><subject>Sensitivity analysis</subject><subject>Studies</subject><subject>Subgroups</subject><subject>Type 2 diabetes</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNk9uK2zAQhk1p6W7TvkFpDYXSXiS1Dpbim8Ky9BBYWOjpVoylSaKgSFnLXrrv1QesnHhDXPai-ELWzDe_NDOaLHtJihlhknzYhK7x4Ga74HFWFFIyKh5l56RidCpowR6f_J9lz2LcFEXJ5kI8zc4oJ1xUUp5nfy4M3nTQorvLwcCuRZNbHztnfR5RN9ja4HPwJjf9DmLyr3EHrdVHDn-3Deg9qKGLmKPDWzhV0sFr9InqoZjMR0-D0cYWfJv74KfGQo29NJgGU3IJ09akSHBhC3l_bNrE59mTJbiIL4Z1kv38_OnH5dfp1fWXxeXF1VSLirZTCVAxQktEYRhQUSAgsoJQItBQxrSuS85pRauSsLTlJSVYU6RzIiSksk2y1wfdnQtRDQWPinDO-JzLtEyyxYEwATZq19gtNHcqgFV7Q2hWCpqUkENVyrmgjEhaF5hOJTU1lWRcIF2ilKbX-jic1tVbNIeCuZHo2OPtWq3CrWIytbLsBd4NAk246TC2amujRufAY-j29-as4pTThL75B304u4FaQUrA-mXoG92Lqgsu55QLLkiiZg9Q6TO4tanzuLTJPgp4PwpITJve0Cq9nagW37_9P3v9a8y-PWHXCK5dx-C6_aMbg_wA6ibE2ODyWGRSqH647quh-uFSw3ClsFenDToG3U8T-wuCYiMq</recordid><startdate>20131016</startdate><enddate>20131016</enddate><creator>Anderwald, Christian-Heinz</creator><creator>Tura, Andrea</creator><creator>Gessl, Alois</creator><creator>Luger, Anton</creator><creator>Pacini, Giovanni</creator><creator>Krebs, Michael</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131016</creationdate><title>Adequately adapted insulin secretion and decreased hepatic insulin extraction cause elevated insulin concentrations in insulin resistant non-diabetic adrenal incidentaloma patients</title><author>Anderwald, Christian-Heinz ; 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However, little is known about beta-cell secretion in AI, because comparisons are difficult, since beta-cell-function varies with altered insulin-sensitivity. To retrospectively analyze beta-cell function in non-diabetic AI, compared to healthy controls (CON). AI (n=217, 34%males, 57 ± 1 years, body-mass-index:27.7 ± 0.3 kg/m(2)) and CON [n = 25, 32%males, 56 ± 1 years, 26.7 ± 0.8 kg/m(2)] with comparable anthropometry (p ≥ 0.31) underwent oral-glucose-tolerance-tests (OGTTs) with glucose, insulin, and C-peptide measurements. 1mg-dexamethasone-suppression-tests were performed in AI. AI were divided according to post-dexamethasone-suppression-test cortisol-thresholds of 1.8 and 5 µg/dL into 3 subgroups: pDexa<1.8 µg/dL, pDexa1.8-5 µg/dL and pDexa>5 µg/dL. Using mathematical modeling, whole-body insulin-sensitivity [Clamp-like-Index (CLIX)], insulinogenic Index, Disposition Index, Adaptation Index, and hepatic insulin extraction were calculated. CLIX was lower in AI combined (4.9 ± 0.2 mg · kg(-1) · min(-1)), pDexa<1.8 µg/dL (4.9 ± 0.3) and pDexa1.8-5 µg/dL (4.7 ± 0.3, p<0.04 vs.CON:6.7 ± 0.4). Insulinogenic and Disposition Indexes were 35%-97% higher in AI and each subgroup (p<0.008 vs.CON), whereas C-peptide-derived Adaptation Index, compensating for insulin-resistance, was comparable between AI, subgroups, and CON. Mathematical estimation of insulin-derived (insulinogenic and Disposition) Indexes from associations to insulin-sensitivity in CON revealed that AI-subgroups had ~19%-32% higher insulin-secretion than expectable. These insulin-secretion-index differences negatively (r=-0.45, p<0.001) correlated with hepatic insulin extraction, which was 13-16% lower in AI and subgroups (p<0.003 vs.CON). AI-patients show insulin-resistance, but adequately adapted insulin secretion with higher insulin concentrations during an OGTT, because of decreased hepatic insulin extraction; this finding affects all AI-patients, regardless of dexamethasone-suppression-test outcome.]]></abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24146977</pmid><doi>10.1371/journal.pone.0077326</doi><tpages>e77326</tpages><oa>free_for_read</oa></addata></record>
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identifier ISSN: 1932-6203
ispartof PloS one, 2013-10, Vol.8 (10), p.e77326-e77326
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1932-6203
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subjects Adaptation
Adrenal Gland Neoplasms - metabolism
Anthropometry
Beta cells
Blood Glucose
Body measurements
C-Peptide - blood
Case-Control Studies
Comparative analysis
Control methods
Cortisol
Dexamethasone
Diabetes mellitus
Female
Glucose
Glucose tolerance
Glucose Tolerance Test
Humans
Insulin
Insulin - blood
Insulin - metabolism
Insulin Resistance
Insulin Secretion
Insulin-Secreting Cells - metabolism
Liver
Liver - metabolism
Male
Males
Mathematical analysis
Mathematical models
Middle Aged
Patients
Peptides
Retrospective Studies
Risk Factors
Rodents
Secretion
Sensitivity
Sensitivity analysis
Studies
Subgroups
Type 2 diabetes
title Adequately adapted insulin secretion and decreased hepatic insulin extraction cause elevated insulin concentrations in insulin resistant non-diabetic adrenal incidentaloma patients
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