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Mitochondrial dysfunction in cardiomyocytes of obese mice
Author(s) -
Moura Aníbal Sanches,
Cortez Erika Costa,
Bernardo Amélia Faustino,
GarciaSouza Érica Patricia,
Neves Fabiana Alves,
Mattos Ana Marcondez,
Miranda Glauciane Lacerda,
Melo Soares Vivian,
Sichieri Rosely
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1028.3
Subject(s) - medicine , endocrinology , bioenergetics , ultrastructure , mitochondrion , biology , nad+ kinase , carnitine , chemistry , biochemistry , anatomy , enzyme
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).