INHIBITION BY GLUCOCORTICOIDS OF PROSTAGLANDIN RELEASE FROM ADIPOSE TISSUE in vitro

Abstract

When rabbit chopped adipose tissue was incubated with a lipolytic agent (adrenocorticotrophic hormone, ACTH1–24, 0.1 μg/ml) in Krebs solution, prostaglandin E2 was formed in the tissue and about the same amount was found in the medium. In the presence of indomethacin (1 μg/ml) the appearance of prostaglandin E2 was almost abolished both in the tissue and in the medium. When the incubation was carried out in the presence of hydrocortisone or betamethasone (1–10 μg/ml) the concentration of prostaglandin E2 leaking or carried into the medium was significantly reduced, whereas that remaining in the tissue was significantly increased. This action of the steroids was not reversed by increasing substrate (arachidonic acid) concentration in the medium. The steroids did not affect lipolysis, nor did they influence prostaglandin metabolism since such activity was not detectable in the adipose tissue. Anti‐inflammatory steroids therefore did not reduce prostaglandin formation but increased the tissue/medium ratio, which supports the view that they inhibit the release of prostaglandins after these have been synthesized.

The Effects of Glucocorticoids on the Distribution and Mobilisation of Arachidonic Acid in Fat Cell Ghosts

“…The prostaglandin release associated with the vasodilatation accompanying lipolysis in rabbit was found to be prevented not only by prostaglandin synthetase inhibitors (Bowery & Lewis, 1973) but also by glucocorticoids (Lewis & Piper, 1975). These findings were confirmed in vitro in adrenocorticotrophic hormone (ACrH)induced lipolysis in rabbit and catecholamine-induced lipolysis in human isolated fat cells (Chang, Lewis & Piper, 1977). Similar findings had also been made in lung tissue stimulated by anaphylaxis or blood vessels constricted with noradrenaline (Gryglewski Panczenko, Korbut, Grodzinska & Ocetkiewicz, 1975).…”

Time Courses of the Anti‐anaphylactic and Anti‐inflammatory Effects of Dexamethasone in the Rat and Mouse

“…The short lag period of dexamethasone in this model, less than 4 h, may reflect an action on the capillary bed or an inhibition of prostaglandin release, which has a very short lag period (Gryglewski, Panczenko. Korbut, Grodzinska & Ocetkiewicz, 1975;Flower, Harvey, Moncada, Nijkamp & Vane, 1976;Chang, Lewis & Piper, 1977).…”

Influences of variation in total energy intake and dietary composition on regulation of fat cell lipolysis in ideal-weight subjects.

“…Prostaglandins of the E-and F-type are produced and released by adipose tissue (35). The physiological role of eicosanoids in regulation of human fat cell function is not known at present.…”