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Type 1 and type 2 diabetes are distinct clinical entities primarily driven by autoimmunity and metabolic dysfunction, respectively. However, there is a growing appreciation that they may share an etiopathological factor, namely the role of variation in beta-cell sensitivity to stress factors. Increased sensitivity increases the risk of beta-cell death or insulin secretion dysfunction. The beta-cell fragility model proposes that this variation contributes to the risk of developing either type 1 or type 2 diabetes, in the presence of immunological and/or metabolic stress factors. Therapeutics that increase the resistance of beta cells to these factors and decreasing fragility may constitute a new class of anti-diabetogenics, with potential use across both diseases.

Original publication

DOI

10.1016/j.molmed.2016.12.005

Type

Journal article

Journal

Trends Mol Med

Publication Date

02/2017

Volume

23

Pages

181 - 194

Keywords

Animals, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Glucose, Humans, Insulin-Secreting Cells, Risk Factors