Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway

Author(s)

Salome de Campos, Dijon Henrique ^[1] ; Leopoldo, Andre Soares ^[2] ; Lima-Leopoldo, Ana Paula ^[2] ; do Nascimento, Andre Ferreira ^[3] ; de Oliveira-Junior, Silvio Assis ^{[1, 4]} ; Tomaz da Silva, Danielle Cristina ^[1] ; Sugizaki, Mario Mateus ^[3] ; Padovani, Carlos Roberto ^[5] ; Cicogna, Antonio Carlos ^[1]

Affiliation

^[1] UNESP, Fac Med Botucatu, Dept Clin Med, BR-18618000 Botucatu, SP - Brazil

^[2] Univ Fed Espirito Santo, Ctr Educ Fis & Desportos, Dept Esportes, Vitoria, ES - Brazil

^[3] Univ Fed Mato Grosso UFMT, Inst Ciencias Saude, Sinop, MT - Brazil

^[4] Univ Fed Mato Grosso UFMS, Escola Fisioterapia, Campo Grande, MS - Brazil

^[5] UNESP, Inst Ciencias Biol, Dept Bioestat, BR-18618000 Botucatu, SP - Brazil

• Document type: Journal article
• Source: Arquivos Brasileiros de Cardiologia; v. 103, n. 4, p. 330-337, OCT 2014.
• Web of Science Citations: 5

Abstract

Background: Obesity is defined by excessive accumulation of body fat relative to lean tissue. Studies during the last few years indicate that cardiac function in obese animals may be preserved, increased or diminished. Objective: Study the energy balance of the myocardium with the hypothesis that the increase in fatty acid oxidation and reduced glucose leads to cardiac dysfunction in obesity. Methods: 30-day-old male Wistar rats were fed standard and hypercaloric diet for 30 weeks. Cardiac function and morphology were assessed. In this paper was viewed the general characteristics and comorbities associated to obesity. The structure cardiac was determined by weights of the heart and left ventricle (LV). Myocardial function was evaluated by studying isolated papillary muscles from the LV, under the baseline condition and after inotropic and lusitropic maneuvers: myocardial stiffness; postrest contraction; increase in extracellular Ca2+ concentration; change in heart rate and inhibitor of glycolytic pathway. Results: Compared with control group, the obese rats had increased body fat and co-morbities associated with obesity. Functional assessment after blocking iodoacetate shows no difference in the linear regression of DT, however, the RT showed a statistically significant difference in behavior between the control and the obese group, most notable being the slope in group C. Conclusion: The energy imbalance on obesity did not cause cardiac dysfunction. On the contrary, the prioritization of fatty acids utilization provides protection to cardiac muscle during the inhibition of glycolysis, suggesting that this pathway is fewer used by obese cardiac muscle. (AU)