Mitochondria in metabolic disease: Getting clues from proteomic studies
Corresponding Author
Juan R. Peinado
Department of Medical Sciences, Faculty of Medicine, Ciudad Real, Spain
Correspondence: Dr. Juan R. Peinado, Department of Medical Sciences, University of Castilla la Mancha, CiudadReal, Spain
E-mail:[email protected]
Fax: + 34 957 21 86 34
Additional corresponding author: Dr. Maria M. Malagon, E-mail: [email protected]
Search for more papers by this authorAlberto Diaz-Ruiz
Department of Cell Biology, Physiology and Immunology, Instituto Maimónides de Investigación Biomédica (IMIBIC), Reina Sofia University Hospital, Universidad de Cordoba, Cordoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
Search for more papers by this authorGema Frühbeck
CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain
Search for more papers by this authorCorresponding Author
Maria M. Malagon
Department of Cell Biology, Physiology and Immunology, Instituto Maimónides de Investigación Biomédica (IMIBIC), Reina Sofia University Hospital, Universidad de Cordoba, Cordoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
Correspondence: Dr. Juan R. Peinado, Department of Medical Sciences, University of Castilla la Mancha, CiudadReal, Spain
E-mail:[email protected]
Fax: + 34 957 21 86 34
Additional corresponding author: Dr. Maria M. Malagon, E-mail: [email protected]
Search for more papers by this authorCorresponding Author
Juan R. Peinado
Department of Medical Sciences, Faculty of Medicine, Ciudad Real, Spain
Correspondence: Dr. Juan R. Peinado, Department of Medical Sciences, University of Castilla la Mancha, CiudadReal, Spain
E-mail:[email protected]
Fax: + 34 957 21 86 34
Additional corresponding author: Dr. Maria M. Malagon, E-mail: [email protected]
Search for more papers by this authorAlberto Diaz-Ruiz
Department of Cell Biology, Physiology and Immunology, Instituto Maimónides de Investigación Biomédica (IMIBIC), Reina Sofia University Hospital, Universidad de Cordoba, Cordoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
Search for more papers by this authorGema Frühbeck
CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain
Search for more papers by this authorCorresponding Author
Maria M. Malagon
Department of Cell Biology, Physiology and Immunology, Instituto Maimónides de Investigación Biomédica (IMIBIC), Reina Sofia University Hospital, Universidad de Cordoba, Cordoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
Correspondence: Dr. Juan R. Peinado, Department of Medical Sciences, University of Castilla la Mancha, CiudadReal, Spain
E-mail:[email protected]
Fax: + 34 957 21 86 34
Additional corresponding author: Dr. Maria M. Malagon, E-mail: [email protected]
Search for more papers by this authorColour Online: See the article online to view Fig. 2 in colour.
Abstract
Mitochondria play a key role as major regulators of cellular energy homeostasis, but in the context of mitochondrial dysfunction, mitochondria may generate reactive oxidative species and induce cellular apoptosis. Indeed, altered mitochondrial status has been linked to the pathogenesis of several metabolic disorders and specially disorders related to insulin resistance, such as obesity, type 2 diabetes, and other comorbidities comprising the metabolic syndrome. In the present review, we summarize information from various mitochondrial proteomic studies of insulin-sensitive tissues under different metabolic states. To that end, we first focus our attention on the pancreas, as mitochondrial malfunction has been shown to contribute to beta cell failure and impaired insulin release. Furthermore, proteomic studies of mitochondria obtained from liver, muscle, and adipose tissue are summarized, as these tissues constitute the primary insulin target metabolic tissues. Since recent advances in proteomic techniques have exposed the importance of PTMs in the development of metabolic disease, we also present information on specific PTMs that may directly affect mitochondria during the pathogenesis of metabolic disease. Specifically, mitochondrial protein acetylation, phosphorylation, and other PTMs related to oxidative damage, such as nitrosylation and carbonylation, are discussed.
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