The metabolic effects of prostaglandins. I. The influence of prostaglandin E-1 on the carbohydrate and lipid metabolism of rat epididymal fatty tissue

Abstract

Prostaglandins are hormone-like substances, which are synthetized in mammals from C20-fatty acids with 3–5 double bonds. Recently it was shown that these substances inhibit the activation of lipolysis in fatty tissue. We have investigated the effect of 0.1μg/ml PGE1 (prostaglandin E1) on the carbohydrate and fat metabolism of isolated epididymal tissue in rats, utilizing glucose-containing buffers with and without addition of 500μU/ml insulin, 0.1μg/ml adrenaline and 25μg/ml human growth hormone. At the above mentioned concentration, PGE1 influenced the basal lipolysis (release of glycerol) to a greater extent than insulin. — The growth hormone- and adrenaline-induced activation of glycerol liberation from fatty acids was decreased by PGE1. The basal oxidation of 1-14C-glucose to14CO2 was stimulated by about 70% through the action of PGE1. This stimulation amounted to nearly one-tenth of the effect of 500μU/ml of insulin. The influence of PGE1 on glucose oxidation could be significantly increased by the addition of adrenaline and growth hormone. Glucose oxidation stimulated by PGE1 amounted to one-third of the stimulation produced by insulin, and corresponded to the effect, of 0.1μg/ml of adrenaline and 25μg/ml of growth hormone. PGE1 only intensified the increase in glucose uptake caused by adrenaline. The effect of growth hormone was not influenced. Addition of PGE1 to the incubation media raised by almost 80% the incorporation of 1-14C-glucose into the lipids of the epididymal fatty tissue; this corresponded to approximately 10% of the effect of insulin, 40% of the effect of adrenaline and 80% that of growth hormone. The effect of the last two hormones was slightly stimulated by the simultaneous addition of PGE1 to the incubation media. These experiments indicate that PGE1 influences both glucose and lipid metabolism in epididymal fatty tissue. It is proposed that the stimulating effect of PGE1 on glucose utilization is a consequence of regulatory changes in cellular metabolism and is closely related to antilipolytic activity.