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The role of cellular calcium homeostasis in the improved contractile function associated with high‐fat feeding in heart failure
Author(s) -
Cheng YiHsin,
McElfresh Tracy A,
Chen Xiaoqin,
Rutledge Cody A,
Chandler Margaret P
Publication year - 2009
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.23.1_supplement.953.5
Subject(s) - contractility , heart failure , medicine , endocrinology , lipotoxicity , endoplasmic reticulum , homeostasis , in vivo , calcium , ligation , cardiology , chemistry , biology , biochemistry , insulin resistance , microbiology and biotechnology , insulin
Heart failure (HF) is characterized by deteriorating left ventricular (LV) function. High saturated fat diets (SAT) are associated with increased risks for lipotoxicity and contractile dysfunction. However, HF animals fed SAT for 8 weeks post coronary artery ligation exhibited improved LV contractility in vivo compared to HF animals fed normal chow (NC). Ca 2+ handling proteins (e.g. sarcoplasmic reticulum (SR) Ca 2+ ATPase) regulate myocardial contractility, and Ca 2+ handling properties (e.g. Ca 2+ transients) are known to be altered in HF. Since SAT improved LV contractility in HF, it is possible that alterations in Ca 2+ handling properties have been restored. Male Wistar rats underwent coronary ligation or sham surgery and fed NC (10% kcal fat) or SAT (60% kcal saturated fat) for 8 weeks. In vivo contractile function was assessed by echocardiography and LV cannulation 7‐8 weeks post surgery. Hearts were harvested and cardiomyocytes were isolated enzymatically, following by measurements of cell shortening (digitally), Ca 2+ transients (with fura‐2AM), and SR Ca 2+ store (by caffeine). Preliminary results suggest that cell shortening, Ca 2+ transients, and SR Ca 2+ store are improved in HF+SAT relative to HF+NC. However, SAT had no effect in sham animals. Thus, high saturated fat diet improves myocardial contractility by reversing altered Ca 2+ handling properties in HF. (Grant: NHLBI HL‐081857 & AHA 0535361N)