The accelerator hypothesis and increasing incidence of type 1 diabetes

Curr Opin Endocrinol Diabetes Obes. 2008 Aug;15(4):321-5. doi: 10.1097/MED.0b013e3283073a5a.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Autoimmunity
  • Diabetes Mellitus, Type 1 / epidemiology*
  • Diabetes Mellitus, Type 1 / etiology*
  • Diabetes Mellitus, Type 1 / immunology
  • Diabetes Mellitus, Type 2 / epidemiology
  • Diabetes Mellitus, Type 2 / immunology
  • Diabetes Mellitus, Type 2 / metabolism
  • Humans
  • Immunity, Innate
  • Incidence
  • Insulin Resistance / immunology
  • Islets of Langerhans / immunology
  • Islets of Langerhans / metabolism
  • Risk Factors