Minimal Model: Perspective from 2005

The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today – both as a clinical tool and an approach to understanding the composite effects of insulin secretion and insulin sensitivity on glucose tolerance and risk for type 2 diabetes melli...

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Published inHormone research Vol. 64; no. Suppl 3; pp. 8 - 15
Main Author Bergman, Richard N.
Format Journal Article
LanguageEnglish
Published Basel, Switzerland 01.01.2005
Subjects
Chromosomes, Human, Pair 11 - genetics
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Glucose Intolerance - genetics
Glucose Intolerance - metabolism
Glucose Intolerance - pathology
Humans
Insulin - metabolism
Insulin Resistance - genetics
Insulin Sensitivity: Methods
Insulin-Secreting Cells - metabolism
Insulin-Secreting Cells - pathology
Models, Biological
Quantitative Trait Loci - genetics
Insulin resistance
Genetics
Modelling
Disposition index
Insulin secretion
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Abstract The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today – both as a clinical tool and an approach to understanding the composite effects of insulin secretion and insulin sensitivity on glucose tolerance and risk for type 2 diabetes mellitus. The original assumptions of the model have led to an understanding of the kinetics of insulin in vivo, as well as the relative importance of β-cell compensatory failure in the pathogenesis of diabetes. The disposition index (DI), a parameter emerging from the model, represents the ability of the pancreatic islets to compensate for insulin resistance. There is evidence that a locus on chromosome 11 codes for the DI, which has a significant heritability and can predict type 2 diabetes better than any known genetic locus. Even today, the model continues to be a subject of scientific discovery and discourse.
AbstractList The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today – both as a clinical tool and an approach to understanding the composite effects of insulin secretion and insulin sensitivity on glucose tolerance and risk for type 2 diabetes mellitus. The original assumptions of the model have led to an understanding of the kinetics of insulin in vivo, as well as the relative importance of β-cell compensatory failure in the pathogenesis of diabetes. The disposition index (DI), a parameter emerging from the model, represents the ability of the pancreatic islets to compensate for insulin resistance. There is evidence that a locus on chromosome 11 codes for the DI, which has a significant heritability and can predict type 2 diabetes better than any known genetic locus. Even today, the model continues to be a subject of scientific discovery and discourse.
The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today - both as a clinical tool and an approach to understanding the composite effects of insulin secretion and insulin sensitivity on glucose tolerance and risk for type 2 diabetes mellitus. The original assumptions of the model have led to an understanding of the kinetics of insulin in vivo, as well as the relative importance of beta-cell compensatory failure in the pathogenesis of diabetes. The disposition index (DI), a parameter emerging from the model, represents the ability of the pancreatic islets to compensate for insulin resistance. There is evidence that a locus on chromosome 11 codes for the DI, which has a significant heritability and can predict type 2 diabetes better than any known genetic locus. Even today, the model continues to be a subject of scientific discovery and discourse.
The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today - both as a clinical tool and an approach to understanding the composite effects of insulin secretion and insulin sensitivity on glucose tolerance and risk for type 2 diabetes mellitus. The original assumptions of the model have led to an understanding of the kinetics of insulin in vivo, as well as the relative importance of beta-cell compensatory failure in the pathogenesis of diabetes. The disposition index (DI), a parameter emerging from the model, represents the ability of the pancreatic islets to compensate for insulin resistance. There is evidence that a locus on chromosome 11 codes for the DI, which has a significant heritability and can predict type 2 diabetes better than any known genetic locus. Even today, the model continues to be a subject of scientific discovery and discourse.The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today - both as a clinical tool and an approach to understanding the composite effects of insulin secretion and insulin sensitivity on glucose tolerance and risk for type 2 diabetes mellitus. The original assumptions of the model have led to an understanding of the kinetics of insulin in vivo, as well as the relative importance of beta-cell compensatory failure in the pathogenesis of diabetes. The disposition index (DI), a parameter emerging from the model, represents the ability of the pancreatic islets to compensate for insulin resistance. There is evidence that a locus on chromosome 11 codes for the DI, which has a significant heritability and can predict type 2 diabetes better than any known genetic locus. Even today, the model continues to be a subject of scientific discovery and discourse.
Author Bergman, Richard N.
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Cites_doi 10.1172%2FJCI110398
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10.1016%2FS0197-2456%2897%2900151-7
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10.1007%2Fs00125-004-1657-3
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Issue Suppl 3
Keywords Insulin resistance
Genetics
Modelling
Disposition index
Insulin secretion
Language English
License Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
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References_xml – reference: Bergman RN: Toward physiological understanding of glucose tolerance: the minimal model approach. Lilly Award Lecture. Diabetes 1989;38:1512-1527.2684710
– reference: Gladwell M: The Tipping Point: How Little Things Can Make a Big Difference. Boston, Little, Brown and Company, 2000.
– reference: Srinivasan R, Kadish AH, Sridhar R: A mathematical model for the control mechanism of free fatty acid-glucose metabolism in normal humans. Comput Biomed Res 1970;3:146-165.543193310.1016%2F0010-4809%2870%2990021-2
– reference: Grodsky GM: A threshold distribution hypothesis for packet storage of insulin and its mathematical modeling. J Clin Invest 1972;51:2047-2059.455994610.1172%2FJCI107011
– reference: Azen SP, Peters RK, Berkowitz K, Kjos S, Xiang A, Buchanan TA: TRIPOD (TRoglitazone In the Prevention Of Diabetes): a randomized, placebo-controlled trial of troglitazone in women with prior gestational diabetes mellitus. Control Clin Trials 1998;19:217-231.955128510.1016%2FS0197-2456%2897%2900151-7
– reference: Bergman RN, Phillips LS, Cobelli C: Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and Β-cell glucose sensitivity from the response to intravenous glucose. J Clin Invest 1981;68:1456-1467.703328410.1172%2FJCI110398
– reference: Topor ZL, Pawlicki M, Remmers JE: A computational model of the human respiratory control system: responses to hypoxia and hypercapnia. Ann Biomed Eng 2004;32:1530-1545.1563611310.1114%2FB%3AABME.0000049037.65204.4c
– reference: Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M; Finnish Diabetes Prevention Study Group: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001;344:1343-1350.1133399010.1056%2FNEJM200105033441801
– reference: Bergman RN, Ider YZ, Bowden CR, Cobelli C: Quantitative estimation of insulin sensitivity. Am J Physiol 1979;236:E667-E677.
– reference: Letiexhe MR, Desaive C, Lefebvre PJ, Scheen AJ: Intact cross-talk between insulin secretion and insulin action after postgastroplasty recovery of ideal body weight in severely obese patients. Int J Obes Relat Metab Disord 2004;28:821-823.1505227810.1038%2Fsj.ijo.0802632
– reference: Guyton AC: Circulatory Physiology: Cardiac Output and Its Regulation. Philadelphia, PA, Saunders, 1963.
– reference: Zethelius B, Lithell H, Hales CN, Berne C: Insulin sensitivity, proinsulin and insulin as predictors of coronary heart disease. A population-based 10-year, follow-up study in 70-year old men using the euglycaemic insulin clamp. Diabetologia 2005;48:862-867.1580333110.1007%2Fs00125-005-1711-9
– reference: Mittleman SD, Van Citters GW, Kim SP, Davis DA, Dea MK, Bergman RN: The longitudinal compensation for fat induced insulin resistance includes reduced insulin clearance and enhanced beta-cell response. Diabetes 2000;49:2116-2125.1111801510.1016/S0140-6736(07)60028-2
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Snippet The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today – both as a clinical tool and an...
The minimal model was proposed over 25 years ago. Despite (or because of) its simplicity it continues to be used today - both as a clinical tool and an...
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SubjectTerms Chromosomes, Human, Pair 11 - genetics
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Glucose Intolerance - genetics
Glucose Intolerance - metabolism
Glucose Intolerance - pathology
Humans
Insulin - metabolism
Insulin Resistance - genetics
Insulin Sensitivity: Methods
Insulin-Secreting Cells - metabolism
Insulin-Secreting Cells - pathology
Models, Biological
Quantitative Trait Loci - genetics
Title Minimal Model: Perspective from 2005
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