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The accelerator hypothesis and increasing incidence of type 1 diabetes

Fourlanos, Spiros; Harrison, Leonard C; Colman, Peter G

Current Opinion in Endocrinology, Diabetes and Obesity: August 2008 - Volume 15 - Issue 4 - p 321–325
doi: 10.1097/MED.0b013e3283073a5a
Diabetes and the endocrine pancreas II: Edited by Peter A. Gottlieb

Purpose of review To summarize the relevance of the ‘accelerator hypothesis’ to type 1 diabetes pathogenesis and examine if recent evidence supports the hypothesis. The ‘accelerator hypothesis’ proposes ‘three processes in type 1 diabetes which variably accelerate the loss of beta cells through apoptosis: constitution, insulin resistance and autoimmunity’.

Recent findings Insulin resistance is an independent risk factor for progression to clinical type 1 diabetes in people with islet autoimmunity. Higher bodyweight is also associated with type 1 diabetes development although no longitudinal studies have simultaneously assessed bodyweight and insulin resistance in preclinical diabetes. Currently, there is no evidence for the view that accelerated beta-cell apoptosis is due to insulin resistance in the pathogenesis of type 1 diabetes.

Summary Insulin resistance accelerates development of type 1 diabetes in people with islet autoimmunity and insulin deficiency. The increasingly ‘obesogenic’ environment which promotes insulin resistance could account for the rising incidence of type 1 diabetes.

Royal Melbourne Hospital, Parkville, Melbourne, VIC, Australia

Correspondence to Dr Spiros Fourlanos, MBBS, FRACP, PhD, Endocrinologist & General Physician, Royal Melbourne Hospital, Grattan Street, Parkville, Melbourne, VIC 3050, Australia E-mail:

© 2008 Lippincott Williams & Wilkins, Inc.