Moura AS FASEB 2011

Moura AS, Cortez E, Bernardo A, Garcia-Souza E, Neves F, Mattos A, Miranda G, Soares V and Sichieri R (2011) Mitochondrial dysfunction in cardiomyocytes of obese mice. JASEB J 25: 1028.3

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Moura AS, Cortez E, Bernardo A, Garcia-Souza E, Neves F, Mattos A, Miranda G, Soares V, Sichieri R (2011)

Event: FASEB J

Cellular energy metabolism is impaired in obesity. Therefore in this study it was investigated cardiomyocyte bioenergetics and ultrastructure of adult obese mice overfed during lactation.

We performed high-resolution respirometry of cardiomyocytes from obese (OG) and control (CG) groups with an Oroboros 2k-Oxygraph. State 2 (absence of ADP), state 3 (ADP-stimulated) and state 4 respiration were examined with NAD-linked substrates or fatty acid. Cardiomyocytes ultrastructure was analyzed by transmission electron microscopy. The content of mitochondrial proteins Carnitine palmitoil transferase 1 (CPT1) and Uncoupling protein 2 (UCP2) was achieved by western blotting. Statistical significance was assessed by analysis of variance (ANOVA) followed by Tukey’s test; P<0.05.

OG presented higher body weight and epididymal fat than CG (P<0.0001). O2 consumption was not different between groups using NAD-linked substrates but significantly lower in OG when palmitoil-carnitine was added as substrate (P<0.0001). CPT1 and UCP2 content was found significantly increased in OG (P<0.05). Ultrastructure analysis showed disrupted mitochondria in OG and also a higher ectopic lipid deposition then CG.

We suggest that early life overnutrition leads to obesity associated with cardiomyocytes bioenergetics and ultrastructure impairment. Supported by CNPq (305903/2007); FAPERJ(E-26/110.578/2009).

• Keywords: obesity; cardiomyocytes;

• O2k-Network Lab: BR Rio de Janeiro Moura AS

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Organism: Mouse  Tissue;cell: Heart  Preparation: Intact cells 

HRR: Oxygraph-2k