Diabetes Mathematical Models

Diabetes mathematical models from our lab are listed below. The models illustrate how diabetes results from the interaction of insulin resistance and impairment of the ability of beta-cells to compensate for it.

View other models from our lab by subject on our Mathematical Models page. Visit GitHub.com to view a list of models by publication citation.

T2D Pathogenesis

This model for the pathogenesis of type 2 diabetes shows that disease onset is a threshold-crossing process, which explains why prevention is easier than cure. One of the predictions of the model is confirmed in the companion experimental paper.

Chronic glucose exposure systematically shifts the oscillatory threshold of mouse islets: Experimental evidence for an early intrinsic mechanism of compensation for hyperglycemia.
Glynn E, Ha J, Kennedy RT, Lu S, Satin LS, Sherman A, Thompson B, Vadrevu S.
Endocrinology. (2016) 157(2):611-623. Abstract/Full Text
Mathematical Model of the Pathogenesis, Prevention and Reversal of Type 2 Diabetes.
Ha J, Satin LS, Sherman AS.
Endocrinology. (2016) 157(2):624-635. Abstract/Full Text
Access on GitHub.com

T2D Pathways

This model accounts for the diversity of pathways typically followed, focusing on two extreme alternatives, one that goes through impaired fasting glucose (IFG) first and one that goes through impaired glucose tolerance (IGT) first. IFG generally results from primarily hepatic insulin resistance, while IGT results primarily from peripheral insulin resistance. We consider whether hyperinsulinemia may be a cause of insulin resistance rather than a consequence and find that this is at best a small effect.

Type 2 Diabetes: One Disease, Many Pathways.
Ha J, Sherman A.
Endocrinol. and Metab. (2020) 319(2):E410-E426. Abstract/Full Text
Access on GitHub.com