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Influence of long‐term exposure of obesity on protein expression of myocardial calcium handling
Author(s) -
LimaLeopoldo Ana Paula,
Leopoldo André,
Sugizaki Mário,
Nascimento André,
Campos Dijon,
Silva Danielle,
Luvizotto Renata,
Alves Carlos,
Freire Paula,
Deus Adriana,
Cicogna Antonio Carlos
Publication year - 2013
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.27.1_supplement.1197.10
Subject(s) - hyperinsulinemia , medicine , endocrinology , obesity , insulin resistance , dyslipidemia , phosphorylation , calcium , phospholamban , cardiology , chemistry , biochemistry
Several structural and functional changes of the heart have often been associated with human obesity and experimental models. Myocardial calcium (Ca2+) handling has been extensively studied in several experimental models and has often been shown to be related to cardiac dysfunction. The objective was to test the hypothesis that the increased duration of exposure to obesity leads to a reduction in the expression and/or phosphorylation of proteins levels related to myocardial Ca2+ handling. The adiposity index used to characterize animals as obese was 79.5%, 82%, and 69.5% higher than controls after 15, 30, and 45 weeks, respectively. Obesity promoted comorbities such as glucose intolerance, insulin resistance, hyperinsulinemia, hyperleptinemia, and dyslipidemia; however, were not associated with changes in systolic blood pressure. The cardiac structure results post‐death showed that obesity caused cardiac hypertrophy at the 3 evaluation times. The obesity was not accompanied by changes in protein expression of L‐type Ca2+ channels, SERCA and CSQ. The protein levels of PLB, PLB phosphorylation at threonine‐17 (pPLB thr17), and the ratio between pPLB thr17 and PLB was not changed due to obesity. The main finding of this study was that obesity, after 15 and 30 weeks, resulted in decreased levels of PLB phosphorylation at serine‐16 (pPPLB ser16).