Two sites of action of steroids on the prostaglandin system

Abstract

When fat cells are stimulated by a lipolytic agent such as ACTH, they are activated in such a way that a series of biochemical steps lead to activation of tissue lipase. The action of this enzyme on triglycerides causes the release of free fatty acids (FFA), among which is presumably arachidonic acid (AA). This is acted on by cyclo-oxygenase to produce endoperoxides, thromboxanes and prostaglandins (PGs). Prostaglandins, at least, have been shown to cause functional vasodilatation in vivo but perhaps some of the other products of the cyclo-oxygenase system also cause vasodilatation. In the experiments in which we examined subcutaneous adipose tissue in rabbits in vivo, FFA release was detected, the vasodilatation measured and the PG formation estimated in tissue extracts, obtained after activation of the adipose tissue by ACTH, and release of PGE₂ into the venous blood measured by radioimmunoassay^1,2. In addition investigations were carried out in chopped fat and isolated fat cells in vitro. FFA and glycerol levels and PG formation during activation of chopped fat and in isolated fat cells in vitro were also measured³.