|Relling, David - UNIV NORTH DAKOTA|
|Esberg, Lucy - UNIV NORTH DAKOTA|
|Murphy, Eric - UNIV NORTH DAKOTA|
|Carlson, Edward - UNIV NORTH DAKOTA|
|Ren, Jun - UNIV WYOMING|
Submitted to: Obesity II
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 21, 2006
Publication Date: May 1, 2007
Repository URL: http://handle.nal.usda.gov/10113/46439
Citation: Relling, D.P., Esberg, L.B., Johnson, W.T., Murphy, E.J., Carlson, E.C., Lukaski, H.C., Saari, J.T., Ren, J. 2007. Dietary interaction of high fat and marginal copper deficiency on cardiac contractile function. Obesity. 15(5):1242-1257. Interpretive Summary: Increased fat intake is associated with obesity and increased risk for cardiovascular disease. Thus, in the industrialized world, the ready availability of high fat convenience foods may increase the risk for cardiovascular disease. However, the risk may be compounded because high fat convenience foods are not a good source of copper and adequate dietary copper intake is also required for optimal cardiovascular health. The present study examined the combined effects of dietary fat and copper on the contractile function of rat heart cells. Results from the study showed that high fat intake and marginal copper intake both impaired the ability of heart cells to contract. However, the effects of high fat and marginal copper intakes were independent of one another. This indicates that marginal copper intake does not influence the negative effect of high fat on heart cell contraction and that lowering fat intake does not influence the negative effect of marginal copper intake on heart cell contraction. In practical terms, lowering fat intake may lower the risk for cardiovascular disease, but optimal reduction in risk may not be achieved unless dietary copper intake is also adequate.
Technical Abstract: High fat and copper deficient diets impair heart function leading to cardio hypertrophy, increased lipid droplet volume and compromised contractile function, resembling liptoxic cardiac dysfunction. However, the combined effect of the two on cardiac function is unknown. The purpose or objective of this study was to determine whether there is an interaction between high fat and copper deficient diets on cardiomyocyte contractile function. Weanling male rats were fed diets incorporating 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 (TPS), time-to-90% relengthening (TR90), maximal velocity of shortening/relengthening (+/- dL/dt), intracellular Ca2+ rise and decay. Neither dietary treatment or intervention affected blood pressure or glucose levels although high fat diet elicited obesity and glucose intolerance. Both diets depressed PS, +/- dL/dt, increased intracellular Ca2+ rise, and prolonged TR90 and CA2+ decay, without additive effect between the two. Ca2+ sensitivity, apoptosis, lipid peroxidation, nitrosative damage, tissue ceramide and triglyceride levels were unaffected by either diet alone or in combination. Phospholamban but not SERCA2a was increased by both diets. eNOS was depressed with additive effect; i.e. interaction. Electron transport chain was unaffected although mitochondrial aconitase activity was inhibited by high fat diet. These data suggest that high fat and copper deficient diets impaired cardiomyocyte contractile function and intracellular Ca2+ homeostasis, possibly through a similar mechanism, without obvious lipotoxicity, nitrosative damage or apoptosis.