Minimal Model: Perspective from 2005

• Published in: Hormone research Vol. 64; no. Suppl 3; pp. 8 - 15
• Main Author: Bergman, Richard N.
• Format: Journal Article
• Language: English
• 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
• ISBN: 3805580630; 9783805580632
• ISSN: 1663-2818; 0301-0163; 1663-2826
• DOI: 10.1159/000089312

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.