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Dietary Interaction of High Fat and Marginal Copper Deficiency on Cardiac Contractile Function

Permanent URL:
http://handle.nal.usda.gov/10113/46439
File:
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Abstract:
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 Ca²⁺ ([Ca²⁺]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 Ca²⁺ ([Ca²⁺]I) rise and prolonged time-to-90% relengthening and Ca²⁺ decay without an additive effect between the two. Ca²⁺ 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 Ca²⁺-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 [Ca²⁺]i homeostasis, possibly through a similar mechanism, without obvious lipotoxicity, nitrosative damage, and apoptosis.
Author(s):
Relling, David P. , Esberg, Lucy B. , Johnson, W. Thomas , Murphy, Eric J. , Carlson, Edward C. , Lukaski, Henry C. , Saari, Jack T. , Ren, Jun
Subject(s):
rats , animal models , weanlings , dietary fat , copper , dietary minerals , nutrient deficiencies , myocardium , muscle contraction , cardiac output , hypertrophy , lipid content , low fat diet , blood pressure , blood glucose , obesity , glucose tolerance , calcium , cations , lipid peroxidation , apoptosis , triacylglycerols , adenosinetriphosphatase
Format:
p. 1242-1257.
Note:
Includes references
Source:
Obesity 2007 May, v. 15, no. 5
Language:
English
Publisher:
The North American Association for the Study of Obesity
Year:
2007
Collection:
Journal Articles, USDA Authors, Peer-Reviewed
Rights:
Works produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. The content of this document is not copyrighted.