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

Fex, Malin LU ; Nicholas, Lisa M. LU ; Vishnu, Neelanjan LU ; Medina, Anya LU ; Sharoyko, Vladimir V. LU ; Nicholls, David G. LU ; Spégel, Peter LU and Mulder, Hindrik LU (2018) In Journal of Endocrinology 236(3). p.145-149
Abstract

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... (More)

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.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Coupling signal, Genetic variation, Mitochondrial transcription, Oxidative phosphorylation, TCA cycle
in
Journal of Endocrinology
volume
236
issue
3
pages
145 - 149
publisher
Society for Endocrinology
external identifiers
  • scopus:85042503452
ISSN
0022-0795
DOI
10.1530/JOE-17-0367
language
English
LU publication?
yes
id
ebb7ee60-3238-4252-9d64-c55cdecb9823
date added to LUP
2018-03-19 11:37:02
date last changed
2019-03-19 03:51:22
@article{ebb7ee60-3238-4252-9d64-c55cdecb9823,
  abstract     = {<p>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.</p>},
  author       = {Fex, Malin and Nicholas, Lisa M. and Vishnu, Neelanjan and Medina, Anya and Sharoyko, Vladimir V. and Nicholls, David G. and Spégel, Peter and Mulder, Hindrik},
  issn         = {0022-0795},
  keyword      = {Coupling signal,Genetic variation,Mitochondrial transcription,Oxidative phosphorylation,TCA cycle},
  language     = {eng},
  number       = {3},
  pages        = {145--149},
  publisher    = {Society for Endocrinology},
  series       = {Journal of Endocrinology},
  title        = {The pathogenetic role of β-cell mitochondria in type 2 diabetes},
  url          = {http://dx.doi.org/10.1530/JOE-17-0367},
  volume       = {236},
  year         = {2018},
}