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 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.
Bergman
Richard N
RN
Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. rbergman@usc.edu
D002880:Chromosomes, Human, Pair 11 / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D018149:Glucose Intolerance / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000235:genetics; D050417:Insulin-Secreting Cells / Q000378:metabolism* / Q000473:pathology; D008954:Models, Biological; D040641:Quantitative Trait Loci / Q000235:genetics
D007328:Insulin