Key result
High-fat and marginally copper-deficient diets impaired cardiomyocyte contractile function and calcium homeostasis without an additive effect between the two.
Why the study?
Does a high-fat and marginally copper-deficient diet impair cardiomyocyte contractile function in weanling male rats?
Does a high-fat and marginally copper-deficient diet impair cardiomyocyte contractile function in weanling male rats?
High-fat and marginally copper-deficient diets independently impair cardiomyocyte contractile function and calcium homeostasis without additive effects or obvious lipotoxicity.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications from this animal study; leaves open human translation of diet effects on cardiac function.
OBJECTIVE: High-fat and marginally copper-deficient diets impair heart function, leading to cardiac hypertrophy, increased lipid droplet volume, and compromised contractile function, resembling lipotoxic cardiac dysfunction. However, the combined effect of the two on cardiac function is unknown. This study was designed to examine the interaction between high-fat and marginally copper-deficient diets on cardiomyocyte contractile function. RESEARCH METHODS AND PROCEDURES: Weanling male rats were fed diets incorporating a low- or high-fat diet (10% or 45% of kcal from fat, respectively) with adequate (6 mg/kg) or marginally deficient (1.5 mg/kg) copper content for 12 weeks. Contractile function was determined with an IonOptix system including peak shortening (PS), time-to-PS, time-to-90% relengthening, maximal velocity of shortening/relengthening, and intracellular Ca(2+) ([Ca(2+)](I)) rise and decay. RESULTS: Neither dietary treatment affected blood pressure or glucose levels, although the high-fat diet elicited obesity and glucose intolerance. Both diets depressed PS, maximal velocity of shortening/relengthening, and intracellular Ca(2+) ([Ca(2+)](I)) rise and prolonged time-to-90% relengthening and Ca(2+) decay without an additive effect between the two. Ca(2+) sensitivity, apoptosis, lipid peroxidation, nitrosative damage, tissue ceramide, and triglyceride levels were unaffected by either diet or in combination. Phospholamban (PLB) but not sarco(endo)plasmic reticulum Ca(2+)-ATPase was increased by both diets. Endothelial NO synthase was depressed with concurrent treatments. The electron transport chain was unaffected, although mitochondrial aconitase activity was inhibited by the high-fat diet. DISCUSSION: These data suggest that high-fat and marginally copper deficient diets impaired cardiomyocyte contractile function and [Ca(2+)](i) homeostasis, possibly through a similar mechanism, without obvious lipotoxicity, nitrosative damage, and apoptosis.
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Relling et al. (2007) studied Cardiac contractile function. High-fat and marginally copper-deficient diets vs. Low-fat (10% kcal from fat) and adequate copper (6 mg/kg) diets was evaluated on Cardiomyocyte contractile function. High-fat and marginally copper-deficient diets impaired cardiomyocyte contractile function and calcium homeostasis without an additive effect between the two.
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