Okumura T, Kanemaki T, Kitade H
Department of Medical Chemistry, Kansai Medical University, Osaka, Japan.
Biochim Biophys Acta. 1993 Mar 10;1176(1-2):137-42. doi: 10.1016/0167-4889(93)90188-u.
In primary cultures of rat hepatocytes, 16,16-dimethylprostaglandin E2 (16,16-dimethyl PGE2), a biologically active analogue of prostaglandin E2 (PGE2), stimulated the basal rate of [14C]glucose incorporation into glycogen. 16,16-Dimethyl PGE2 caused concentration-dependent stimulation (ED50: 10(-8) M) with a maximum 2-3 h after its addition. Prostaglandin E1 (PGE1), PGE2 and prostaglandin F2 alpha (PGF2 alpha) stimulated also the incorporation, but less effectively than 16,16-dimethyl PGE2. However, prostaglandin D2 (PGD2) did not show such effect. Cellular glycogen analysis revealed that PGE2 and 16,16-dimethyl PGE2 increased a net glycogen accumulation time-dependently. Pretreatment of the cultured hepatocytes with pertussis toxin blocked the effects of PGE2 and 16,16-dimethyl PGE2 completely and concentration-dependently. These findings indicate that E-series prostaglandins have significant effects on hepatic glycogenesis via pertussis-toxin-sensitive G protein, in addition to their inhibitory effects on hormone-stimulated glycogenolysis reported previously (Okumura, T., Sago, T. and Saito, K. (1988) Prostaglandins 36, 463-475).
在大鼠肝细胞原代培养物中，16,16 - 二甲基前列腺素E2（16,16 - dimethyl PGE2），一种前列腺素E2（PGE2）的生物活性类似物，刺激了[14C]葡萄糖掺入糖原的基础速率。16,16 - 二甲基PGE2引起浓度依赖性刺激（半数有效浓度：10(-8) M），在添加后2 - 3小时达到最大值。前列腺素E1（PGE1）、PGE2和前列腺素F2α（PGF2α）也刺激了掺入，但效果不如16,16 - 二甲基PGE2。然而，前列腺素D2（PGD2）未显示出这种作用。细胞糖原分析显示，PGE2和16,16 - 二甲基PGE2随时间依赖性地增加了糖原的净积累。用百日咳毒素预处理培养的肝细胞完全且浓度依赖性地阻断了PGE2和16,16 - 二甲基PGE2的作用。这些发现表明，除了它们先前报道的对激素刺激的糖原分解的抑制作用外（奥村，T.，佐古，T.和斋藤，K.（1988年）前列腺素36，463 - 475），E系列前列腺素通过百日咳毒素敏感的G蛋白对肝糖原生成有显著影响。
