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Transcribing β-cell mitochondria in health and disease

Mulder, Hindrik LU (2017) In Molecular Metabolism 6(9). p.1040-1051
Abstract

Background: The recent genome-wide association studies (GWAS) of Type 2 Diabetes (T2D) have identified the pancreatic β-cell as the culprit in the pathogenesis of the disease. Mitochondrial metabolism plays a crucial role in the processes controlling release of insulin and β-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.... (More)

Background: The recent genome-wide association studies (GWAS) of Type 2 Diabetes (T2D) have identified the pancreatic β-cell as the culprit in the pathogenesis of the disease. Mitochondrial metabolism plays a crucial role in the processes controlling release of insulin and β-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 β-cells in health and disease.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Expression quantitative trait locus (eQTL), Genome-wide association study (GWAS), Insulin secretion, Islets, Mitochondria, β-Cell
in
Molecular Metabolism
volume
6
issue
9
pages
1040 - 1051
publisher
Elsevier GmbH
external identifiers
  • scopus:85020678498
ISSN
2212-8778
DOI
10.1016/j.molmet.2017.05.014
language
English
LU publication?
yes
id
1df88ca5-0a18-43e8-b251-b7bcf41f4556
date added to LUP
2017-07-04 14:17:35
date last changed
2018-03-11 04:41:31
@article{1df88ca5-0a18-43e8-b251-b7bcf41f4556,
  abstract     = {<p>Background: The recent genome-wide association studies (GWAS) of Type 2 Diabetes (T2D) have identified the pancreatic β-cell as the culprit in the pathogenesis of the disease. Mitochondrial metabolism plays a crucial role in the processes controlling release of insulin and β-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 β-cells in health and disease.</p>},
  author       = {Mulder, Hindrik},
  issn         = {2212-8778},
  keyword      = {Expression quantitative trait locus (eQTL),Genome-wide association study (GWAS),Insulin secretion,Islets,Mitochondria,β-Cell},
  language     = {eng},
  month        = {05},
  number       = {9},
  pages        = {1040--1051},
  publisher    = {Elsevier GmbH},
  series       = {Molecular Metabolism},
  title        = {Transcribing β-cell mitochondria in health and disease},
  url          = {http://dx.doi.org/10.1016/j.molmet.2017.05.014},
  volume       = {6},
  year         = {2017},
}