AJP - Heart and Circulatory Physiology, Vol 248, Issue 2 208-H216, Copyright © 1985 by American Physiological Society

ARTICLES

Stimulation of lipolysis in rat heart myocytes by isoproterenol

A. Kryski Jr, K. A. Kenno and D. L. Severson

Calcium-tolerant myocytes were isolated from rat hearts. Isoproterenol produced a dose-dependent increase in glycerol output (lipolysis) that could be blocked by propranolol. The presence of glucose in the incubation medium enhanced the release of glycerol from myocytes but had no effect on the decline in triacylglycerol content. No incorporation of radioactivity from [U-14C]glucose into glycerol could be detected. In incubations with isoproterenol, there was a stoichiometric relationship between the glycerol output and the decrease in triacylglycerol levels. The addition of the phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine resulted in an increase in the basal glycerol output and an enhancement of the isoproterenol-stimulated lipolytic rate. Forskolin and 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate also produced a concentration-dependent stimulation of lipolysis in myocytes. Therefore, lipolysis in isolated myocytes must be regulated by adenosine 3',5'-cyclic monophosphate-dependent mechanisms. These results demonstrate that lipolysis can be observed in myocardial cells and that the lipolytic response to isoproterenol cannot be secondary to a physiological (inotropic) response since these myocyte preparations are quiescent.

This article has been cited by other articles:

				D. An, G. Kewalramani, D. Qi, T. Pulinilkunnil, S. Ghosh, A. Abrahani, R. Wambolt, M. Allard, S. M. Innis, and B. Rodrigues {beta}-Agonist stimulation produces changes in cardiac AMPK and coronary lumen LPL only during increased workload Am J Physiol Endocrinol Metab, June 1, 2005; 288(6): E1120 - E1127. [Abstract] [Full Text] [PDF]