Journal
MOLECULAR METABOLISM
Volume 6, Issue 9, Pages 1040-1051Publisher
ELSEVIER
DOI: 10.1016/j.molmet.2017.05.014
Keywords
beta-Cell; Mitochondria; Islets; Genome-wide association study (GWAS); Insulin secretion; Expression quantitative trait locus (eQTL)
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Funding
- Swedish Research Council
- European Foundation for the Study of Diabetes
- Swedish Diabetes
- Novo Nordisk Foundation
- Albert Pahlsson Foundation
- Diabetes Wellness
- Swedish Foundation for Strategic Research
- Medical Faculty in Lund, Sweden
- Novo Nordisk Fonden [NNF14OC0010591] Funding Source: researchfish
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Background: The recent genome-wide association studies (GWAS) of Type 2 Diabetes (T2D) have identified the pancreatic beta-cell as the culprit in the pathogenesis of the disease. Mitochondrial metabolism plays a crucial role in the processes controlling release of insulin and beta-cell mass. This notion implies that mechanisms controlling mitochondrial function have the potential to play a decisive pathogenetic role in T2D. Scope of the review: This article reviews studies demonstrating that there is indeed mitochondrial dysfunction in islets in T2D, and that GWAS have identified a variant in the gene encoding transcription factor B1 mitochondrial (TFB1M), predisposing to T2D due to mitochondrial dysfunction and impaired insulin secretion. Mechanistic studies of the nature of this pathogenetic link, as well as of other mitochondrial transcription factors, are described. Major conclusions: Based on this, it is argued that transcription and translation in mitochondria are critical processes determining mitochondrial function in beta-cells in health and disease. (C) 2017 The Author. Published by Elsevier GmbH.
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