Intracellular origin and regulation of endogenous lipolysis in rat heart.
The rate of glycerol release from isolated, perfused rat hearts was used as an index for endogenous lipolysis. Pharmacological and metabolic interventions were performed in order to obtain information about the intracellular site of action and regulation of tissue triglyceride (TG) hydrolysis in heart. It proved that endogenous lipolysis probably is of lysosomal origin. The activity of tissue lipolysis is dependent on the amount of stored TG and on the contractile status of the heart and is subject to feedback inhibition by production of fatty acids. Evidence is presented that Ca2+ plays an important role in the regulation and hormonal modification of lipolysis since all mechanisms inducing alterations in Ca2+ homeostasis influence myocardial lipolysis. Our experimental data and current knowledge are discussed in the light of a new hypothesis which relates intracellular Ca2+ and the rate of fatty acid utilization to the activity (activities) of tissue lipase(s). It is proposed that inhibition of endogenous lipolysis may be the main mechanism of action of antiarrhythmic agents (lidocaine, quinidine, phenothiazines).
D000818:Animals; D001826:Body Fluids / Q000201:enzymology*; D002118:Calcium / Q000378:metabolism; D004036:Diet, Atherogenic; D005227:Fatty Acids / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D005991:Glycerol Kinase / Q000378:metabolism; D007424:Intracellular Fluid / Q000201:enzymology*; D008066:Lipolysis; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology*; D051381:Rats; D011919:Rats, Inbred Strains; D014280:Triglycerides / Q000378:metabolism
D005227:Fatty Acids; D014280:Triglycerides; D005991:Glycerol Kinase; D005990:Glycerol; D002118:Calcium