Okumura T, Saito K
Department of Medical Chemistry, Kansai Medical School, Osaka, Japan.
Prostaglandins. 1990 May;39(5):525-40. doi: 10.1016/0090-6980(90)90035-t.
16,16-Dimethylprostaglandin E2 (dimethylPGE2) increased the incorporation 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, dimethylPGE2, prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha), but not prostaglandin D2 (PGD2), 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 identical conditions except for the presence of glucagon, isoproterenol (beta-adrenergic response) or epinephrine (with propranolol, alpha 1-adrenergic response), dimethylPGE2 and PGE2 inhibited hormone-stimulated glycogenolysis but again PGD2 had no effect.
16,16-二甲基前列腺素E2（二甲基PGE2）可增加原代培养的大鼠肝细胞中葡萄糖掺入糖原的量，其刺激作用可被用百日咳毒素预处理细胞所阻断。相反，二甲基PGE2、前列腺素E2（PGE2）和前列腺素F2α（PGF2α），但不是前列腺素D2（PGD2），可抑制胰岛素诱导的糖原生成中的葡萄糖掺入，并且这些抑制作用不会被百日咳毒素预处理所阻断。前列腺素和其他刺激物（脂多糖、血小板活化因子、佛波酯和酵母聚糖）不会增加[14C]糖原标记的肝细胞中[14C]葡萄糖的释放。另一方面，在除了存在胰高血糖素、异丙肾上腺素（β-肾上腺素能反应）或肾上腺素（与普萘洛尔一起，α1-肾上腺素能反应）之外的相同条件下，二甲基PGE2和PGE2可抑制激素刺激的糖原分解，但PGD2同样没有作用。
