Mitochondrial quality control systems sustain brain mitochondrial bioenergetics in early stages of type 2 diabetes

R X Santos, S C Correia, M G Alves, P F Oliveira, S Cardoso, C Carvalho, R Seiça, M S Santos, P I Moreira*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)


Mitochondria have a crucial role in the supply of energy to the brain. Mitochondrial alterations can lead to detrimental consequences on the function of brain cells and are thought to have a pivotal role in the pathogenesis of several neurologic disorders. This study was aimed to evaluate mitochondrial function, fusion-fission and biogenesis and autophagy in brain cortex of 6-month-old Goto-Kakizaki (GK) rats, an animal model of nonobese type 2 diabetes (T2D). No statistically significant alterations were observed in mitochondrial respiratory chain and oxidative phosphorylation system. A significant decrease in the protein levels of OPA1, a protein that facilitates mitochondrial fusion, was observed in brain cortex of GK rats. Furthermore, a significant decrease in the protein levels of LC3-II and a significant increase in protein levels of mTOR phosphorylated at serine residue 2448 were observed in GK rats suggesting a suppression of autophagy in diabetic brain cortex. No significant alterations were observed in the parameters related to mitochondrial biogenesis. Altogether, these results demonstrate that during the early stages of T2D, brain mitochondrial function is maintained in part due to a delicate balance between mitochondrial fusion-fission and biogenesis and autophagy. However, future studies are warranted to evaluate the role of mitochondrial quality control pathways in late stages of T2D.

Original languageEnglish
Pages (from-to)13-22
Number of pages10
JournalMolecular & Cellular Biochemistry
Issue number1-2
Early online date16 May 2014
Publication statusPublished - Sept 2014

Bibliographical note

Renato X. Santos has a PhD fellowship from the Fundação para a Ciência e a Tecnologia (SFRH/BD/43972/2008).


  • Animals
  • Autophagy
  • Cerebral Cortex/metabolism
  • Diabetes Mellitus, Type 2/metabolism
  • Disease Models, Animal
  • Disease Progression
  • Energy Metabolism
  • GTP Phosphohydrolases/metabolism
  • Microtubule-Associated Proteins/metabolism
  • Mitochondria/metabolism
  • Mitochondrial Dynamics
  • Mitochondrial Turnover
  • Phosphorylation
  • Rats
  • Rats, Wistar
  • TOR Serine-Threonine Kinases/metabolism
  • Time Factors


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