Mitochondria and diabetes: An intriguing pathogenetic role
Mitochondria play a key role in energy metabolism and ATP production in many tissues, including skeletal muscle, cardiac muscle, brain and liver. Inherent disorders of mitochondria such as mDNA deletions cause major disruption of metabolism and can result in severe disease phenotypes. However, the...
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| Format: | Book Chapter |
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Springer New York LLC
2012
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| Online Access: | http://hdl.handle.net/20.500.11937/29670 |
| _version_ | 1848752867118153728 |
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| author | Newsholme, Philip Gaudel, C. Krause, M. |
| author2 | Scatena, Roberto |
| author_facet | Scatena, Roberto Newsholme, Philip Gaudel, C. Krause, M. |
| author_sort | Newsholme, Philip |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | Mitochondria play a key role in energy metabolism and ATP production in many tissues, including skeletal muscle, cardiac muscle, brain and liver. Inherent disorders of mitochondria such as mDNA deletions cause major disruption of metabolism and can result in severe disease phenotypes. However, the incidence of such mDNA based disorders is extremely rare and cannot account for the dramatic rise in human metabolic diseases, which are characterised by defects in energy metabolism. Mitochondrial dysfunction characterised by reduced ATP generation and reduced mitochondrial number in skeletal muscle or reduced ATP generation and mitochondrial stimulus-secretion coupling in the pancreatic beta cell has been implicated in the pathology of chronic metabolic disease associated with type 2 diabetes mellitus and also with aging. Additionally the generation of ROS from mitochondria and other cellular sources may interfere in insulin signaling in muscle, contributing to insulin resistance. Reduced mitochondrial oxidative capacity coupled with increased ROS generation underlies the accumulation of intramuscular fat, insulin resistance and muscle dysfunction in aging. We will review the molecular basis for optimal mitochondrial function or mechanisms of dysfunction and correlate with pathology of identified diseases and aging. |
| first_indexed | 2025-11-14T08:15:26Z |
| format | Book Chapter |
| id | curtin-20.500.11937-29670 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-14T08:15:26Z |
| publishDate | 2012 |
| publisher | Springer New York LLC |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-296702023-02-07T08:01:18Z Mitochondria and diabetes: An intriguing pathogenetic role Newsholme, Philip Gaudel, C. Krause, M. Scatena, Roberto Bottoni, Patrizia Giardina Bruno insulin resistance and diabetes muscle dysfunction in aging reactive oxygen species (ROS) mitochondrial dysfunction mitochondrial DNA Mitochondria play a key role in energy metabolism and ATP production in many tissues, including skeletal muscle, cardiac muscle, brain and liver. Inherent disorders of mitochondria such as mDNA deletions cause major disruption of metabolism and can result in severe disease phenotypes. However, the incidence of such mDNA based disorders is extremely rare and cannot account for the dramatic rise in human metabolic diseases, which are characterised by defects in energy metabolism. Mitochondrial dysfunction characterised by reduced ATP generation and reduced mitochondrial number in skeletal muscle or reduced ATP generation and mitochondrial stimulus-secretion coupling in the pancreatic beta cell has been implicated in the pathology of chronic metabolic disease associated with type 2 diabetes mellitus and also with aging. Additionally the generation of ROS from mitochondria and other cellular sources may interfere in insulin signaling in muscle, contributing to insulin resistance. Reduced mitochondrial oxidative capacity coupled with increased ROS generation underlies the accumulation of intramuscular fat, insulin resistance and muscle dysfunction in aging. We will review the molecular basis for optimal mitochondrial function or mechanisms of dysfunction and correlate with pathology of identified diseases and aging. 2012 Book Chapter http://hdl.handle.net/20.500.11937/29670 10.1007/978-94-007-2869-1_10 Springer New York LLC restricted |
| spellingShingle | insulin resistance and diabetes muscle dysfunction in aging reactive oxygen species (ROS) mitochondrial dysfunction mitochondrial DNA Newsholme, Philip Gaudel, C. Krause, M. Mitochondria and diabetes: An intriguing pathogenetic role |
| title | Mitochondria and diabetes: An intriguing pathogenetic role |
| title_full | Mitochondria and diabetes: An intriguing pathogenetic role |
| title_fullStr | Mitochondria and diabetes: An intriguing pathogenetic role |
| title_full_unstemmed | Mitochondria and diabetes: An intriguing pathogenetic role |
| title_short | Mitochondria and diabetes: An intriguing pathogenetic role |
| title_sort | mitochondria and diabetes: an intriguing pathogenetic role |
| topic | insulin resistance and diabetes muscle dysfunction in aging reactive oxygen species (ROS) mitochondrial dysfunction mitochondrial DNA |
| url | http://hdl.handle.net/20.500.11937/29670 |