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Peral 2017 Abstract MITOEAGLE Barcelona

From Bioblast

Adipocyte mitochondrial dysfunction in aging and diabetes: a redox proteomics approach.

Link: MitoEAGLE

Gomez-Serrano M, Camafeita E, Rubio MA, Torres A, Vazquez J, Peral B (2017)

Event: MitoEAGLE Barcelona 2017


Human age-related diseases, including obesity and type 2 diabetes (T2DM), have long been associated to mitochondrial dysfunction and oxidative stress. We have previously linked obesity to the down-regulation of mitochondrial functions [1,2]. In this work we have tackled the impact of aging and T2DM on adipocyte mitochondria from obese patients by quantitating not only the corresponding abundance changes of proteins, but also the redox alterations undergone by Cys residues thereof [3]. The alterations undergone by the mitochondrial proteome revealed aging- and T2DM-specific hallmarks. Thus, while a global decrease of oxidative phosphorylation (OXPHOS) subunits was found in aging, diabetic patients exhibited a reduction of specific OXPHOS complexes as well as an up-regulation of the anti-oxidant response. Under both conditions, evidence is shown for the first time of a link between increased thiol protein oxidation and decreased protein abundance in adipose tissue mitochondria. This association was stronger in T2DM, where OXPHOS mitochondrial- vs. nuclear-encoded protein modules were found altered, suggesting impaired mitochondrial protein translocation and complex assembly. The marked down-regulation of OXPHOS oxidized proteins and the alteration of certain oxidized Cys residues related to protein import through the redox-active MIA (Mitochondrial Intermembrane space Assembly) pathway support that defects in protein translocation to the mitochondria may be an important underlying mechanism for mitochondrial dysfunction in T2DM also related to physiological aging.

Bioblast editor: Kandolf G

Labels: MiParea: mt-Medicine  Pathology: Aging;senescence, Diabetes, Obesity 

Organism: Human  Tissue;cell: Fat 

Event: B3 


Inst Investigaciones Biomédicas, Alberto Sols (IIBM), (CSIC); Lab Cardiovascular Proteomics, Centro Nacional Investigaciones Cardiovasculares (CNIC); Hospital Clínico San Carlos (IDISSC); Madrid. Spain


  1. Pérez-Pérez R, García-Santos E, Ortega-Delgado FJ, López JA, Camafeita E, Ricart W, Fernández-Real JM, Peral B (2012) Attenuated metabolism is a hallmark of obesity as revealed by comparative proteomic analysis of human omental adipose tissue. J Proteomics 75:783-95.
  2. Gómez-Serrano M, Camafeita E, García-Santos E, López JA, Rubio MA, Sánchez-Pernaute A, Torres A, Vázquez J, Peral B (2016) Proteome-wide alterations on adipose tissue from obese patients as age-, diabetes- and gender-specific hallmarks. Sci Rep 6:25756
  3. Gómez-Serrano M, Camafeita E, López JA, Rubio MA, Bretón I, García-Consuegra I, García-Santos E, Lago J, Sánchez-Pernaute A, Torres A, Vázquez J, Peral B (2016) Differential proteomic and oxidative profiles unveil dysfunctional protein import to adipocyte mitochondria in obesity-associated aging and diabetes. Redox Biol 11:415-28.