Disposition index

The Disposition index (DI) is a measure for the loop gain of the insulin-glucose feedback control system.

[5] Loss of function of the beta cells, reducing their capacity to compensate for insulin resistance, results in a lower disposition index.

[3] The disposition index can be obtained on the basis of data that provide information on insulin sensitivity and beta cell function.

Suitable sources include: If clamp investigations are used the disposition index is defined as the product of the area under the insulin response curve (

[6] Determining the disposition index on the basis of an FSIGT requires fitting the timeseries of insulin and glucose concentrations to the minimal model of insulin-glucose homeostasis.

[10] Based on an oral glucose tolerance test a disposition index can be calculated with

[7][8] The fasting-based disposition index (SPINA-DI) can be obtained from the product of the secretory capacity of pancreatic beta cells (

[9] Disposition index is used as a measure of beta cell function and the ability of the body to dispose of a glucose load.

Thus a lowering of disposition index predicts the conversion of insulin resistance to diabetes mellitus type 2.

[14] Disposition index can be increased by aerobic exercise, but only to the extent that insulin sensitivity is improved.

[15] In a longitudinal evaluation of the NHANES study, a large sample of the general US population, over 10 years, a reduced static disposition index (SPINA-DI) significantly predicted all-cause mortality.

Hyberbolic relationship between insulin sensitivity and beta cell function showing dynamical compensation in "healthy" insulin resistance (transition from A to B) and the evolution of type 2 diabetes mellitus (transition from A to C).
Hyberbolic relationship between insulin sensitivity and beta cell function showing dynamical compensation in "healthy" insulin resistance (transition from A to B) and the evolution of type 2 diabetes mellitus (transition from A to C). Disposition metrics integrate beta cell function and insulin sensitivity in a way so that the results remain constant across dynamical compensation. Changed from Cobelli et al. 2007 and Hannon et al. 2018 [ 1 ] [ 2 ]