ABSTRACT
An increase in the supply and oxidation of free fatty acids (FFA) of endogenous or exogenous origin is one of the characteristic disorders of diabetes. It is postulated that FFA can exert adverse electrophysiological, biochemical, and mechanical effects in the heart. The main criticisms against their involvement in effecting relaxation by lowering cytoplasmic calcium concentration are based on their low affinity for that ion, as well as the very slow rate in which they transport physiological levels of intracellular calcium. Despite these observations, the calcium-accumulating activity of mitochondria may act as a reservoir or "sink" to modulate intracellular calcium stores when concentrations of calcium are pathologically elevated. Both the Na+-Ca2+-exchanger and Ca2+-pump of sarcolemma have been reported to be defective in the diabetic myocardium and, therefore, appear to be involved in the altered calcium transport in the heart during this pathological condition. In animal models, diabetes is produced by injection of chemical agents like alloxan or streptozotocin (STZ).
