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Research Article Free access | 10.1172/JCI106146
1Division of Biological and Medical Sciences, Brown University, Providence, Rhode Island 02912
Find articles by Moskowitz, J. in: JCI | PubMed | Google Scholar
1Division of Biological and Medical Sciences, Brown University, Providence, Rhode Island 02912
Find articles by Fain, J. in: JCI | PubMed | Google Scholar
Published October 1, 1969 - More info
Prostaglandin E1 (PGE1) at a concentration of 1 ng/ml antagonized theophylline, and norepinephrine induced release of glycerol and free fatty acids (FFA) in human fat cell preparations. Insulin at higher doses also inhibited theophylline-stimulated lipolysis. The N6-2-0′dibutyryl derivative of cyclic adenosine monophosphate (DCAMP) stimulated lipolysis. Prostaglandin E1 did not significantly inhibit the lipid mobilizing effects of DCAMP. Changes in glycogen phosphorylase activity after treatment with theophylline, norepinephrine, DCAMP, and PGE1 paralleled those of lipolysis. These results suggest that in man as in experimental animals lipolysis and phosphorylase activity are regulated through processes involving cyclic AMP and that PGE1 appears to exert its antilipolytic effect in human fat cells, as in rat fat cells, by interfering at the level of adenyl cyclase with the accumulation of cyclic AMP.