Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes
Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes Vijay Jayagopal , MRCP 1 , Eric S. Kilpatrick , MRCPATH 2 , Paul E. Jennings , FRCP 1 3 , David A. Hepburn , FRCP 1 and Stephen L. Atkin , FRCP 1 1 Department of Medicine, University of Hull, Hull, U.K...
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| Veröffentlicht in: | Diabetes care 2002-11, Vol.25 (11), p.2022-2025 |
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| creator | JAYAGOPAL, Vijay KILPATRICK, Eric S JENNINGS, Paul E HEPBURN, David A ATKIN, Stephen L |
| description | Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes
Vijay Jayagopal , MRCP 1 ,
Eric S. Kilpatrick , MRCPATH 2 ,
Paul E. Jennings , FRCP 1 3 ,
David A. Hepburn , FRCP 1 and
Stephen L. Atkin , FRCP 1
1 Department of Medicine, University of Hull, Hull, U.K
2 Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, U.K
3 Department of Medicine, York District General Hospital, York, U.K
Abstract
OBJECTIVE —Individuals with type 2 diabetes are particularly vulnerable to cardiovascular disease. Insulin resistance is a major determinant
of this increased risk and is a potential therapeutic target. This study was undertaken to establish the natural biological
variation of insulin resistance in individuals with type 2 diabetes.
RESEARCH DESIGN AND METHODS —The biological variation of insulin resistance was assessed by measuring insulin resistance at 4-day intervals on 10 consecutive
occasions in 12 postmenopausal women with diet-controlled type 2 diabetes and in 11 weight- and age-matched postmenopausal
women without type 2 diabetes. Insulin resistance was derived using the homeostasis model assessment for insulin resistance
(HOMA-IR) method.
RESULTS —The distribution of HOMA-IR was log Gaussian in the type 2 diabetic study group and Gaussian in the control group. The HOMA-IR
in the type 2 diabetic group was significantly greater than that of the control group (mean ± SD: 4.33 ± 2.3 vs. 2.11 ± 0.79
units, P = 0.001). After accounting for analytical variation, the mean intraindividual variation was also substantially greater in
the type 2 diabetic group than in the control group (mean 1.05 vs. 0.15, P = 0.001). Consequently, at any level of HOMA-IR, a subsequent sample must increase by >90% or decrease by >47% to be considered
significantly different from the first.
CONCLUSIONS —HOMA-IR is significantly greater and more variable for individuals with type 2 diabetes. Therefore, this inherent variability
needs to be accounted for in studies evaluating therapeutic reduction of HOMA-IR in this group.
HOMA-IR, homeostasis model assessment for insulin resistance
Footnotes
Address correspondence and reprint requests to Dr. V. Jayagopal, Michael White Centre for Diabetes and Endocrinology, Brocklehurst
Building, Hull Royal Infirmary, 220-236 Anlaby Rd., Hull, HU3 2RW, U.K. E-mail: v.jaygopal{at}hull.ac.uk .
Received for publication 7 February 2002 and accepted in revised form 22 July 2002.
A table elsewhere in this issue |
| doi_str_mv | 10.2337/diacare.25.11.2022 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_gale_infotracacademiconefile_A94142246</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A94142246</galeid><sourcerecordid>A94142246</sourcerecordid><originalsourceid>FETCH-LOGICAL-c511t-a5cf07e5975edc323dc299b8d6ebbb48f165219fcc343318ec7f2113704e6d233</originalsourceid><addsrcrecordid>eNptkV1rFDEUhoModrv6B7yQQbA3OmtOPubjcm3VFiqCVG9DJjnZpsxMtsmM0n9vyg4UZMlFyOE5eU_yEPIG6IZxXn-yXhsdccPkBmDDKGPPyApaLkspRfOcrCiItpRty07IaUp3lFIhmuYlOQEmKNSSrkj32Yc-7LzRffFbR68nH8YiuOIyDBjSpJNPxfdgsS-2KWFKA45TeYHR_0FbXI1p7v1Y_MSMTXo0WOTTzcMeC1ZceN3hhOkVeeF0n_D1sq_Jr69fbs4vy-sf367Ot9elkQBTqaVxtEbZ1hKt4Yxbw9q2a2yFXdeJxkElGbTOGC44hwZN7RgAr6nAyuYPWZOzw737GO5nTJMafDLY93rEMCdVswpqDjKD7_4D78IcxzybYowCyDqnr8nHA7TTPSo_ujBFbXY4YtR9GNH5XN62AgRjosp4eQTPy-LgzTGeHXgTQ0oRndpHP-j4oICqR7tqsauYVADq0W5uersMPncD2qeWRWcG3i-ATtmoi1mJT0-c4FV-XZO5Dwfu1u9u__qcYhdZx2L_AatTvIE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>220115732</pqid></control><display><type>article</type><title>Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>JAYAGOPAL, Vijay ; KILPATRICK, Eric S ; JENNINGS, Paul E ; HEPBURN, David A ; ATKIN, Stephen L</creator><creatorcontrib>JAYAGOPAL, Vijay ; KILPATRICK, Eric S ; JENNINGS, Paul E ; HEPBURN, David A ; ATKIN, Stephen L</creatorcontrib><description>Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes
Vijay Jayagopal , MRCP 1 ,
Eric S. Kilpatrick , MRCPATH 2 ,
Paul E. Jennings , FRCP 1 3 ,
David A. Hepburn , FRCP 1 and
Stephen L. Atkin , FRCP 1
1 Department of Medicine, University of Hull, Hull, U.K
2 Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, U.K
3 Department of Medicine, York District General Hospital, York, U.K
Abstract
OBJECTIVE —Individuals with type 2 diabetes are particularly vulnerable to cardiovascular disease. Insulin resistance is a major determinant
of this increased risk and is a potential therapeutic target. This study was undertaken to establish the natural biological
variation of insulin resistance in individuals with type 2 diabetes.
RESEARCH DESIGN AND METHODS —The biological variation of insulin resistance was assessed by measuring insulin resistance at 4-day intervals on 10 consecutive
occasions in 12 postmenopausal women with diet-controlled type 2 diabetes and in 11 weight- and age-matched postmenopausal
women without type 2 diabetes. Insulin resistance was derived using the homeostasis model assessment for insulin resistance
(HOMA-IR) method.
RESULTS —The distribution of HOMA-IR was log Gaussian in the type 2 diabetic study group and Gaussian in the control group. The HOMA-IR
in the type 2 diabetic group was significantly greater than that of the control group (mean ± SD: 4.33 ± 2.3 vs. 2.11 ± 0.79
units, P = 0.001). After accounting for analytical variation, the mean intraindividual variation was also substantially greater in
the type 2 diabetic group than in the control group (mean 1.05 vs. 0.15, P = 0.001). Consequently, at any level of HOMA-IR, a subsequent sample must increase by >90% or decrease by >47% to be considered
significantly different from the first.
CONCLUSIONS —HOMA-IR is significantly greater and more variable for individuals with type 2 diabetes. Therefore, this inherent variability
needs to be accounted for in studies evaluating therapeutic reduction of HOMA-IR in this group.
HOMA-IR, homeostasis model assessment for insulin resistance
Footnotes
Address correspondence and reprint requests to Dr. V. Jayagopal, Michael White Centre for Diabetes and Endocrinology, Brocklehurst
Building, Hull Royal Infirmary, 220-236 Anlaby Rd., Hull, HU3 2RW, U.K. E-mail: v.jaygopal{at}hull.ac.uk .
Received for publication 7 February 2002 and accepted in revised form 22 July 2002.
A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
DIABETES CARE</description><identifier>ISSN: 0149-5992</identifier><identifier>EISSN: 1935-5548</identifier><identifier>DOI: 10.2337/diacare.25.11.2022</identifier><identifier>PMID: 12401750</identifier><identifier>CODEN: DICAD2</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>Biological and medical sciences ; Diabetes ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetes. Impaired glucose tolerance ; Diet, Diabetic ; Drug resistance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; England ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; European Continental Ancestry Group ; Female ; Homeostasis ; Humans ; Insulin ; Insulin Resistance ; Measurement ; Medical sciences ; Middle Aged ; Models, Biological ; Pathology ; Physiological aspects ; Postmenopause ; Reference Values ; Reproducibility of Results ; Type 2 diabetes</subject><ispartof>Diabetes care, 2002-11, Vol.25 (11), p.2022-2025</ispartof><rights>2003 INIST-CNRS</rights><rights>COPYRIGHT 2002 American Diabetes Association</rights><rights>Copyright American Diabetes Association Nov 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-a5cf07e5975edc323dc299b8d6ebbb48f165219fcc343318ec7f2113704e6d233</citedby><cites>FETCH-LOGICAL-c511t-a5cf07e5975edc323dc299b8d6ebbb48f165219fcc343318ec7f2113704e6d233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14361578$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12401750$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JAYAGOPAL, Vijay</creatorcontrib><creatorcontrib>KILPATRICK, Eric S</creatorcontrib><creatorcontrib>JENNINGS, Paul E</creatorcontrib><creatorcontrib>HEPBURN, David A</creatorcontrib><creatorcontrib>ATKIN, Stephen L</creatorcontrib><title>Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes</title><title>Diabetes care</title><addtitle>Diabetes Care</addtitle><description>Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes
Vijay Jayagopal , MRCP 1 ,
Eric S. Kilpatrick , MRCPATH 2 ,
Paul E. Jennings , FRCP 1 3 ,
David A. Hepburn , FRCP 1 and
Stephen L. Atkin , FRCP 1
1 Department of Medicine, University of Hull, Hull, U.K
2 Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, U.K
3 Department of Medicine, York District General Hospital, York, U.K
Abstract
OBJECTIVE —Individuals with type 2 diabetes are particularly vulnerable to cardiovascular disease. Insulin resistance is a major determinant
of this increased risk and is a potential therapeutic target. This study was undertaken to establish the natural biological
variation of insulin resistance in individuals with type 2 diabetes.
RESEARCH DESIGN AND METHODS —The biological variation of insulin resistance was assessed by measuring insulin resistance at 4-day intervals on 10 consecutive
occasions in 12 postmenopausal women with diet-controlled type 2 diabetes and in 11 weight- and age-matched postmenopausal
women without type 2 diabetes. Insulin resistance was derived using the homeostasis model assessment for insulin resistance
(HOMA-IR) method.
RESULTS —The distribution of HOMA-IR was log Gaussian in the type 2 diabetic study group and Gaussian in the control group. The HOMA-IR
in the type 2 diabetic group was significantly greater than that of the control group (mean ± SD: 4.33 ± 2.3 vs. 2.11 ± 0.79
units, P = 0.001). After accounting for analytical variation, the mean intraindividual variation was also substantially greater in
the type 2 diabetic group than in the control group (mean 1.05 vs. 0.15, P = 0.001). Consequently, at any level of HOMA-IR, a subsequent sample must increase by >90% or decrease by >47% to be considered
significantly different from the first.
CONCLUSIONS —HOMA-IR is significantly greater and more variable for individuals with type 2 diabetes. Therefore, this inherent variability
needs to be accounted for in studies evaluating therapeutic reduction of HOMA-IR in this group.
HOMA-IR, homeostasis model assessment for insulin resistance
Footnotes
Address correspondence and reprint requests to Dr. V. Jayagopal, Michael White Centre for Diabetes and Endocrinology, Brocklehurst
Building, Hull Royal Infirmary, 220-236 Anlaby Rd., Hull, HU3 2RW, U.K. E-mail: v.jaygopal{at}hull.ac.uk .
Received for publication 7 February 2002 and accepted in revised form 22 July 2002.
A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
DIABETES CARE</description><subject>Biological and medical sciences</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diet, Diabetic</subject><subject>Drug resistance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>England</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>European Continental Ancestry Group</subject><subject>Female</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Measurement</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Models, Biological</subject><subject>Pathology</subject><subject>Physiological aspects</subject><subject>Postmenopause</subject><subject>Reference Values</subject><subject>Reproducibility of Results</subject><subject>Type 2 diabetes</subject><issn>0149-5992</issn><issn>1935-5548</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkV1rFDEUhoModrv6B7yQQbA3OmtOPubjcm3VFiqCVG9DJjnZpsxMtsmM0n9vyg4UZMlFyOE5eU_yEPIG6IZxXn-yXhsdccPkBmDDKGPPyApaLkspRfOcrCiItpRty07IaUp3lFIhmuYlOQEmKNSSrkj32Yc-7LzRffFbR68nH8YiuOIyDBjSpJNPxfdgsS-2KWFKA45TeYHR_0FbXI1p7v1Y_MSMTXo0WOTTzcMeC1ZceN3hhOkVeeF0n_D1sq_Jr69fbs4vy-sf367Ot9elkQBTqaVxtEbZ1hKt4Yxbw9q2a2yFXdeJxkElGbTOGC44hwZN7RgAr6nAyuYPWZOzw737GO5nTJMafDLY93rEMCdVswpqDjKD7_4D78IcxzybYowCyDqnr8nHA7TTPSo_ujBFbXY4YtR9GNH5XN62AgRjosp4eQTPy-LgzTGeHXgTQ0oRndpHP-j4oICqR7tqsauYVADq0W5uersMPncD2qeWRWcG3i-ATtmoi1mJT0-c4FV-XZO5Dwfu1u9u__qcYhdZx2L_AatTvIE</recordid><startdate>20021101</startdate><enddate>20021101</enddate><creator>JAYAGOPAL, Vijay</creator><creator>KILPATRICK, Eric S</creator><creator>JENNINGS, Paul E</creator><creator>HEPBURN, David A</creator><creator>ATKIN, Stephen L</creator><general>American Diabetes Association</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>7RV</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0R</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20021101</creationdate><title>Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes</title><author>JAYAGOPAL, Vijay ; KILPATRICK, Eric S ; JENNINGS, Paul E ; HEPBURN, David A ; ATKIN, Stephen L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-a5cf07e5975edc323dc299b8d6ebbb48f165219fcc343318ec7f2113704e6d233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Biological and medical sciences</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diet, Diabetic</topic><topic>Drug resistance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>England</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>European Continental Ancestry Group</topic><topic>Female</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin Resistance</topic><topic>Measurement</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Models, Biological</topic><topic>Pathology</topic><topic>Physiological aspects</topic><topic>Postmenopause</topic><topic>Reference Values</topic><topic>Reproducibility of Results</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JAYAGOPAL, Vijay</creatorcontrib><creatorcontrib>KILPATRICK, Eric S</creatorcontrib><creatorcontrib>JENNINGS, Paul E</creatorcontrib><creatorcontrib>HEPBURN, David A</creatorcontrib><creatorcontrib>ATKIN, Stephen L</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>Nursing & Allied Health Database</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agricultural Science Database</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JAYAGOPAL, Vijay</au><au>KILPATRICK, Eric S</au><au>JENNINGS, Paul E</au><au>HEPBURN, David A</au><au>ATKIN, Stephen L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes</atitle><jtitle>Diabetes care</jtitle><addtitle>Diabetes Care</addtitle><date>2002-11-01</date><risdate>2002</risdate><volume>25</volume><issue>11</issue><spage>2022</spage><epage>2025</epage><pages>2022-2025</pages><issn>0149-5992</issn><eissn>1935-5548</eissn><coden>DICAD2</coden><abstract>Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes
Vijay Jayagopal , MRCP 1 ,
Eric S. Kilpatrick , MRCPATH 2 ,
Paul E. Jennings , FRCP 1 3 ,
David A. Hepburn , FRCP 1 and
Stephen L. Atkin , FRCP 1
1 Department of Medicine, University of Hull, Hull, U.K
2 Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, U.K
3 Department of Medicine, York District General Hospital, York, U.K
Abstract
OBJECTIVE —Individuals with type 2 diabetes are particularly vulnerable to cardiovascular disease. Insulin resistance is a major determinant
of this increased risk and is a potential therapeutic target. This study was undertaken to establish the natural biological
variation of insulin resistance in individuals with type 2 diabetes.
RESEARCH DESIGN AND METHODS —The biological variation of insulin resistance was assessed by measuring insulin resistance at 4-day intervals on 10 consecutive
occasions in 12 postmenopausal women with diet-controlled type 2 diabetes and in 11 weight- and age-matched postmenopausal
women without type 2 diabetes. Insulin resistance was derived using the homeostasis model assessment for insulin resistance
(HOMA-IR) method.
RESULTS —The distribution of HOMA-IR was log Gaussian in the type 2 diabetic study group and Gaussian in the control group. The HOMA-IR
in the type 2 diabetic group was significantly greater than that of the control group (mean ± SD: 4.33 ± 2.3 vs. 2.11 ± 0.79
units, P = 0.001). After accounting for analytical variation, the mean intraindividual variation was also substantially greater in
the type 2 diabetic group than in the control group (mean 1.05 vs. 0.15, P = 0.001). Consequently, at any level of HOMA-IR, a subsequent sample must increase by >90% or decrease by >47% to be considered
significantly different from the first.
CONCLUSIONS —HOMA-IR is significantly greater and more variable for individuals with type 2 diabetes. Therefore, this inherent variability
needs to be accounted for in studies evaluating therapeutic reduction of HOMA-IR in this group.
HOMA-IR, homeostasis model assessment for insulin resistance
Footnotes
Address correspondence and reprint requests to Dr. V. Jayagopal, Michael White Centre for Diabetes and Endocrinology, Brocklehurst
Building, Hull Royal Infirmary, 220-236 Anlaby Rd., Hull, HU3 2RW, U.K. E-mail: v.jaygopal{at}hull.ac.uk .
Received for publication 7 February 2002 and accepted in revised form 22 July 2002.
A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
DIABETES CARE</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>12401750</pmid><doi>10.2337/diacare.25.11.2022</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Diabetes Diabetes Mellitus, Type 2 - physiopathology Diabetes. Impaired glucose tolerance Diet, Diabetic Drug resistance Endocrine pancreas. Apud cells (diseases) Endocrinopathies England Etiopathogenesis. Screening. Investigations. Target tissue resistance European Continental Ancestry Group Female Homeostasis Humans Insulin Insulin Resistance Measurement Medical sciences Middle Aged Models, Biological Pathology Physiological aspects Postmenopause Reference Values Reproducibility of Results Type 2 diabetes |
| title | Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes |
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