The pathogenetic role of β-cell mitochondria in type 2 diabetes

Malin Fex, Lisa M. Nicholas, Neelanjan Vishnu, Anya Medina, Vladimir V. Sharoyko, David G. Nicholls, Peter Spégel, Hindrik Mulder

Research output: Contribution to journalReview articlepeer-review

45 Citations (SciVal)


Mitochondrial metabolism is a major determinant of insulin secretion from pancreatic β-cells. Type 2 diabetes evolves when β-cells fail to release appropriate amounts of insulin in response to glucose. This results in hyperglycemia and metabolic dysregulation. Evidence has recently been mounting that mitochondrial dysfunction plays an important role in these processes. Monogenic dysfunction of mitochondria is a rare condition but causes a type 2 diabetes-like syndrome owing to β-cell failure. Here, we describe novel advances in research on mitochondrial dysfunction in the β-cell in type 2 diabetes, with a focus on human studies. Relevant studies in animal and cell models of the disease are described. Transcriptional and translational regulation in mitochondria are particularly emphasized. The role of metabolic enzymes and pathways and their impact on β-cell function in type 2 diabetes pathophysiology are discussed. The role of genetic variation in mitochondrial function leading to type 2 diabetes is highlighted. We argue that alterations in mitochondria may be a culprit in the pathogenetic processes culminating in type 2 diabetes.

Original languageEnglish
Pages (from-to)R145-R149
JournalJournal of Endocrinology
Issue number3
Publication statusPublished - 2018

Subject classification (UKÄ)

  • Endocrinology and Diabetes


  • Coupling signal
  • Genetic variation
  • Mitochondrial transcription
  • Oxidative phosphorylation
  • TCA cycle


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