Invited Review

Journal of Molecular Medicine

, Volume 81, Issue 8, pp 455-470

First online:

Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes

  • Marc Y. DonathAffiliated withDivision of Endocrinology and Diabetes, University Hospital Email author 
  • , Joachim StørlingAffiliated withSteno Diabetes Center
  • , Kathrin MaedlerAffiliated withDivision of Endocrinology and Diabetes, University Hospital
  • , Thomas Mandrup-PoulsenAffiliated withSteno Diabetes CenterDepartment of Molecular Medicine, Rolf Luft Center for Diabetes Research, Karolinska Institute

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Pancreatic islet β-cell death occurs in type 1 and 2 diabetes mellitus, leading to absolute or relative insulin deficiency. β-cell death in type 1 diabetes is due predominantly to autoimmunity. In type 2 diabetes β-cell death occurs as the combined consequence of increased circulating glucose and saturated fatty acids together with adipocyte secreted factors and chronic activation of the innate immune system. In both diabetes types intra-islet inflammatory mediators seem to trigger a final common pathway leading to β-cell apoptosis. Therefore anti-inflammatory therapeutic approaches designed to block β-cell apoptosis could be a significant new development in type 1 and 2 diabetes.


Apoptosis Interleukin 1 Mitogen-activated protein kinase Jun N-terminal kinase Extracellular signal-regulated kinase