Permissive effects on adipose tissue lipolysis of a plasmatic factor which inhibits prostaglandin biosynthesis.

Plasma obtained from fasted rats provoked a dose-dependent stimulation of fat cell glycerol release and was able to inhibit also generation of prostaglandins E2 and F2 alpha from arachidonate, in vitro, over a very similar range of doses. It is proposed, therefore, that a plasmatic fat-mobilizing factor may act as an endogenous inhibitor of adipose tissue prostaglandin biosynthesis, mediating in the acute (long-term not precluded) regulation of adipose tissue lipolysis. The proposed mechanism of permissive effects of the plasmatic factor in reducing the effects of endogenously-generated inhibitory prostaglandins may be implicated in the development of obesity by reduced availability of the factor and thus reduced ability to utilize fat stores.