Inhibition of glucagon-stimulated hepatic glycogenolysis by E-series prostaglandins.
The effect of E-series prostaglandins (PGE) on hepatic glucose metabolism is controversial. This study uses isolated rat hepatocytes and exogenously added PGE analogs or frequent native PGE additions (to compensate for hepatic PGE degradation) to define PGE's effect on hepatic glycogenolysis. 16,16-Dimethyl PGE2, 15(S),15-methyl PGE2, PGE1 and PGE2 all inhibit glucagon-stimulated glycogenolysis. It is concluded that E-series prostaglandins can act directly on the liver to inhibit glycogenolysis.
D000527:Alprostadil; D000818:Animals; D015232:Dinoprostone / Q000031:analogs & derivatives; D005934:Glucagon / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D011458:Prostaglandins E / Q000494:pharmacology*; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D008112:Liver Glycogen; D011458:Prostaglandins E; D011459:Prostaglandins E, Synthetic; C032514:17,17-dimethylprostaglandin E2; D005934:Glucagon; D000527:Alprostadil; D015232:Dinoprostone