title: Myocardial dysfunction and abnormalities in intracellular calcium handling in obese rats.
abstract: BACKGROUND
  Several mechanisms have been proposed to contribute to cardiac dysfunction in obesity models, such as alterations in calcium (Ca²⁺) handling proteins and β-adrenergic receptors. Nevertheless, the role of these factors in the development of myocardial dysfunction induced by obesity is still not clear.
  
  
  OBJECTIVE
  The purpose of this study was to investigate whether obesity induced by hypercaloric diets results in cardiac dysfunction. Furthermore, it was evaluated whether this functional abnormality in obese rats is related to abnormal Ca²⁺ handling and the β-adrenoceptor system.
  
  
  METHODS
  Male 30-day-old Wistar rats were fed with standard food (C) and a cycle of five hypercaloric diets (Ob) for 15 weeks. Obesity was defined as increases in body fat percentage in rats. Cardiac function was evaluated by isolated analysis of the left ventricle papillary muscle under basal conditions and after inotropic and lusitropic maneuvers.
  
  
  RESULTS
  Compared with the control group, the obese rats had increased body fat and glucose intolerance. The muscles of obese rats developed similar baseline data, but the myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca²⁺ were compromised. There were no changes in cardiac function between groups after β-adrenergic stimulation.
  
  
  CONCLUSIONS
  Obesity promotes cardiac dysfunction related to changes in intracellular Ca²⁺ handling. This functional damage is probably caused by reduced cardiac sarcoplasmic reticulum Ca²⁺ ATPase (SERCA2) activation via Ca²⁺ calmodulin kinase.
authors.affiliation: Departamento de Desportos, Centro de Educação Física e Desportos, UFES-Universidade Federal do Espírito Santo, Vitória, ES.
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Lima-Leopoldo
authors.forename: André S
authors.initials: AS
authors.lastname: Leopoldo
authors.forename: Mário M
authors.initials: MM
authors.lastname: Sugizaki
authors.forename: Alessandro
authors.initials: A
authors.lastname: Bruno
authors.forename: André F
authors.initials: AF
authors.lastname: Nascimento
authors.forename: Renata A M
authors.initials: RA
authors.lastname: Luvizotto
authors.forename: Silvio A de
authors.initials: SA
authors.lastname: Oliveira Júnior
authors.forename: Edson
authors.initials: E
authors.lastname: Castardeli
authors.forename: Carlos R
authors.initials: CR
authors.lastname: Padovani
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Cicogna
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002118:Calcium / Q000378:metabolism*; D004195:Disease Models, Animal; D002149:Energy Intake / Q000502:physiology; D006321:Heart / Q000503:physiopathology; D008297:Male; D023421:Models, Animal; D009206:Myocardium / Q000378:metabolism*; D009765:Obesity / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D011943:Receptors, Adrenergic, beta; D002118:Calcium