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.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D005990:Glycerol / Q000378:metabolism; D008053:Lipid Mobilization / Q000187:drug effects; D008066:Lipolysis; D010455:Peptides / Q000097:blood* / Q000494:pharmacology; D011458:Prostaglandins E / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D011460:Prostaglandins F / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D051381:Rats
D010455:Peptides; D011458:Prostaglandins E; D011460:Prostaglandins F; C008287:lipid mobilizing substance; D005990:Glycerol