Prostacyclin and lipolysis in rat fat cells

Abstract

In rat fat cells incubated for 15 min at 37° and pH 8.5, glycerol release was highly stimulated both by norepinephrine and by theophylline. Prostacyclin (PGI 2) (10 −8−10 −7M) did not alter the basal rate of glycerol release but potentiated the lipolytic effect of 2 × 10 −6M norepinephrine. The rate of norepinephrine-induced glycerol release was increased by PGI 2 during 10 min of incubation and then maintained for the next 5 min. Lipolysis induced by concentrations of norepinephrine which produced maximal effects was not altered by PGI 2. PGI 2 (10 −7−10 −6 M) also potentiated the effect of 5 × 10 −4 M theophylline on glycerol release, but antagonized the stimulation induced by a maximally effective concentration of the methylxanthine (2 × 10 −3M). Incubation of the cells with norepinephrine in the presence of 2 × 10 −4 or 5 × −4 M theophylline caused a loss of the potentiating effect of PGI 2 on norepinephrine-induced lipolysis. In the presence of 10 −3M theophylline, the lipolytic action of norepinephrine was inhibited by PGI 2. In fat cells incubated with adenosine deaminase (0.5 U/ml), 2.5 × 10 −7M PGI 2 did not alter the response to 5 × 10 −4M theophylline and inhibited the effect of norepinephrine both in the absence and in the presence of theophylline. The present results show that, under appropriate experimental conditions, PGI 2 may act as a lipolytic agent in isolated fat cells and that some kind of interaction exists between stimulation of methylxanthine-sensitive adenosine receptors and stimulation of PGI 2 receptors.