Erucic acid‐induced alteration of cardiac triglyceride hydrolysis

Male Wistar rats were fed for 3 or 10 days with high erucic acid rapeseed oil (HEAR) or trierucate (TE). These diets produced increased myocardial triglyceride (TG) levels. Cardiac lipid accumulation was related to basal‐and hormone‐ (glucagon, norepinephrine) stimulated lipolysis, determined as glycerol release, which proved to be enhanced in isolated, perfused hearts from HEAR‐ and TE‐fed rats. Endogenous TG levels in isolated hearts from rats fed the stock and the sunflowerseed oil (SSO) diet were low and probably rate‐limiting for tissue lipolytic activities. HEAR feeding of rats did not modify the rate of erucic acid (22∶1) oxidation in heart. Prolonged HEAR and TE feeding led to a decrease in the endogenous TG level, a process in which the increased rate of TG hydrolysis might play an important role. The enhanced breakdown of tissue TG in hearts from TE‐and HEAR‐fed rats was accompanied by an increased release of fatty acids into the coronary effluent. Erucic acid was a major constituent of the perfusate fatty acids. Evidence is presented that the site of the intracellular TG breakdown is associated with lysosomes, since a subcellular fraction enriched in acid lipase, N‐acetyl‐β‐glucosaminidase and TG could be isolated from heart homogenates of TE‐fed rats. Fatty acids seemed to be an important regulator of tissue lipase activity: palmitate inhibited glucagon‐stimulated lipolysis, which suggests the tissue lipase is subject to product inhibition by fatty acids.