Pajuelo-Reguera 2013 Abstract MiP2013

From Bioblast
Revision as of 11:20, 28 April 2017 by Beno Marija (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision β†’ (diff)
Pajuelo DR, JeΕΎek P, OlejΓ‘r T, AlΓ‘n L (2013) Some mitophagy markers in liver and skeletal muscle in Goto Kakizaki rats. Mitochondr Physiol Network 18.08.


David Pajuelo-Reguera

MiP2013, Book of Abstracts Open Access

Pajuelo D, Jezek P, Olejar T, Alan L (2013)

Event: MiPNet18.08_MiP2013

Diabetes is the epidemic of the XXI century, it is estimated that worldwide 3.2 million deaths are attributable to diabetes every year. It has been described that the severity of insulin resistance in skeletal muscle in type 2 diabetes and obesity is associate with alterations in mitochondrial function [1]. The Goto-Kakizaki (GK) rat is a non-obese Wistar substrain which develops type 2 diabetes mellitus early in life. These rats have been used by the scientific community as it is one of the models to study the relationship between mitochondria and type 2 diabetes mellitus.

The present study was focused on evaluation of the contribution of mitophagy/autophagy in the development of type 2 diabetes in the two most important metabolic tissues in Goto Kakizaki rats. Liver and skeletal muscle tissues were obtained from 1-year old adult male Goto Kakizaki rats and Wistar rats (as controls) of the same age. The samples were analyzed by Western blot. LC3b protein expression and total ubiquitinated protein were used as markers to evaluate mitophagy. The results showed different profiles depending on the tissue. In liver, we observed a ratio LC3bI/LC3bII significantly higher in Goto Kakizaki than Wistar rats, indicating less autophagy activation in the liver of Goto Kakizaki rats. In contrast, the levels of total ubiquitinated protein did not differ significantly. In the case of skeletal muscle, LC3bI/LC3bII levels in Goto Kakizaki were significantly lower than in Wistar rats, indicating increased mitophagy activation in Goto Kakizaki muscle, while the levels of total ubiquitinated protein were not significantly different.

β€’ O2k-Network Lab: CZ Prague Jezek P

Labels: Pathology: Diabetes 

Organism: Rat  Tissue;cell: Skeletal muscle, Liver 

MiP2013, Mitophagy 

Affiliations and author contributions

Dept of Membrane Transport Biophysics, No. 75, Institute of Physiology, v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic. - Email:

Supported within the project The Centre of Biomedical Research (CZ.1.07/2.3.00/30.0025), co-funded by the European Social Fund and the state budget of the Czech Republic.


  1. Zorzano A, Liesa M, PalacΓ­n M (2009) Role of mitochondrial dynamics protein in the pathophysiology of obesity and type 2 diabetes. Int J Biochem Cell Biol 41: 1846-1854.

Cookies help us deliver our services. By using our services, you agree to our use of cookies.