The pathogenetic role of β-cell mitochondria in type 2 diabetes
(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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- author
- 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
- organization
-
- Diabetes - Molecular Metabolism (research group)
- Celiac Disease and Diabetes Unit (research group)
- Genetic and Molecular Epidemiology (research group)
- Department of Experimental Medical Science
- Translational Muscle Research (research group)
- Centre for Analysis and Synthesis
- EXODIAB: Excellence of Diabetes Research in Sweden
- publishing date
- 2018
- 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
- pmid:29431147
- 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
- 2024-09-16 18:55:23
@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}}, keywords = {{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}}, doi = {{10.1530/JOE-17-0367}}, volume = {{236}}, year = {{2018}}, }