Volume 14, Issue 4-5 p. 452-466
Review

Mitochondria in metabolic disease: Getting clues from proteomic studies

Juan R. Peinado

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]

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Alberto Diaz-Ruiz

Alberto 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

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Gema Frühbeck

Gema 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

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Maria M. Malagon

Corresponding 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]

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First published: 12 December 2013
Citations: 45

Colour 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.