Abstract
16, 16-Dimethylprostaglandin E 2 (dimethyl PGE 2) increased the incroporation of glucose into glycogen in rat hepatocytes in primary culture and its stimulatory effect was blocked by pretreatment of the cells with pertussis toxin. In contrast, dimethyl PGE 2, prostaglandin E 2 (PGE 2) and prostaglandin F 2α (PGF 2α), but not prostaglandin D 2 (PGD 2), inhibited glucose incorporation in insulin-induced glycogenesis, and these inhibitory effects were not blocked by pretreatment with pertussis toxin. Prostaglandins and other stimuli (lipopolysaccharide, platelet-activating factor, phorbol ester and zymosan) did not increase the release of [ 14C] glucose from [ 14C] glycogen-labeled hepatocytes. On the other hand, under indentical conditions except for the presence of glucogan, isoproterenol (β-adrenergic response) or epinephrine (with proporanolol, α 1-adrenergic response), dimethyl PGE 2 and PGE 2 inhibited hormone-stimulated glycogenolysis but again PGD 2 had no effect.
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