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Mitochondrial dysfunction in pancreatic beta-cells in Type 2 Diabetes.

Mulder, Hindrik LU orcid and Ling, Charlotte LU (2009) In Molecular and Cellular Endocrinology 297. p.34-40
Abstract
Mitochondrial metabolism controls insulin secretion from the pancreatic beta-cell. Type 2 Diabetes evolves when the beta-cells fail to release appropriate amounts of insulin, causing metabolic dysregulation and hyperglycemia. It is attractive to assume that mitochondrial dysfunction plays a decisive role in these processes. Indeed, while being a rare condition, genetically determined dysfunction of mitochondria causes a Type 2 Diabetes-like syndrome. Here, we review what is known about mitochondrial dysfunction in the beta-cell in Type 2 Diabetes. The focus is on observations in humans but relevant studies in animal models of the disease are discussed. A particular emphasis is placed on changes in metabolic enzymes and function in... (More)
Mitochondrial metabolism controls insulin secretion from the pancreatic beta-cell. Type 2 Diabetes evolves when the beta-cells fail to release appropriate amounts of insulin, causing metabolic dysregulation and hyperglycemia. It is attractive to assume that mitochondrial dysfunction plays a decisive role in these processes. Indeed, while being a rare condition, genetically determined dysfunction of mitochondria causes a Type 2 Diabetes-like syndrome. Here, we review what is known about mitochondrial dysfunction in the beta-cell in Type 2 Diabetes. The focus is on observations in humans but relevant studies in animal models of the disease are discussed. A particular emphasis is placed on changes in metabolic enzymes and function in beta-cell mitochondria and how altered structure of the organelle appears to facilitate its function. These molecular processes are subject to tight genetic as well as epigenetic control. Variations and implications of these mechanisms are reviewed. The emerging picture is that alterations in mitochondria may be a culprit in the pathogenetic processes culminating in Type 2 Diabetes. Such processes may prove to be targets for therapeutic interventions in the disease. (Less)
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type
Contribution to journal
publication status
published
subject
in
Molecular and Cellular Endocrinology
volume
297
pages
34 - 40
publisher
Elsevier
external identifiers
  • wos:000262600600006
  • pmid:18606489
  • scopus:57749185452
  • pmid:18606489
ISSN
1872-8057
DOI
10.1016/j.mce.2008.05.015
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Diabetes and Endocrinology (013241530), Molecular Metabolism (013212001)
id
38f382c6-b9a3-498c-b63d-2a4edb518070 (old id 1181492)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18606489?dopt=Abstract
date added to LUP
2016-04-04 08:22:00
date last changed
2021-07-13 04:18:32
@article{38f382c6-b9a3-498c-b63d-2a4edb518070,
  abstract     = {Mitochondrial metabolism controls insulin secretion from the pancreatic beta-cell. Type 2 Diabetes evolves when the beta-cells fail to release appropriate amounts of insulin, causing metabolic dysregulation and hyperglycemia. It is attractive to assume that mitochondrial dysfunction plays a decisive role in these processes. Indeed, while being a rare condition, genetically determined dysfunction of mitochondria causes a Type 2 Diabetes-like syndrome. Here, we review what is known about mitochondrial dysfunction in the beta-cell in Type 2 Diabetes. The focus is on observations in humans but relevant studies in animal models of the disease are discussed. A particular emphasis is placed on changes in metabolic enzymes and function in beta-cell mitochondria and how altered structure of the organelle appears to facilitate its function. These molecular processes are subject to tight genetic as well as epigenetic control. Variations and implications of these mechanisms are reviewed. The emerging picture is that alterations in mitochondria may be a culprit in the pathogenetic processes culminating in Type 2 Diabetes. Such processes may prove to be targets for therapeutic interventions in the disease.},
  author       = {Mulder, Hindrik and Ling, Charlotte},
  issn         = {1872-8057},
  language     = {eng},
  pages        = {34--40},
  publisher    = {Elsevier},
  series       = {Molecular and Cellular Endocrinology},
  title        = {Mitochondrial dysfunction in pancreatic beta-cells in Type 2 Diabetes.},
  url          = {http://dx.doi.org/10.1016/j.mce.2008.05.015},
  doi          = {10.1016/j.mce.2008.05.015},
  volume       = {297},
  year         = {2009},
}