Fisher R A, Shukla S D, Debuysere M S, Hanahan D J, Olson M S
J Biol Chem. 1984 Jul 25;259(14):8685-8.
The effect of acetylglyceryl ether phosphorylcholine (AGEPC) on glycogenolysis and phosphatidylinositol 4,5-bisphosphate has been studied in rat hepatocytes. Previously, this laboratory demonstrated that AGEPC stimulated glucose output from the perfused rat liver and promoted the breakdown of phosphoinositides in rat hepatocytes (Shukla, S. D., Buxton, D. B., Olson, M.S., and Hanahan, D.J. (1983) J. Biol. Chem. 258, 10212-10214). In the present study, addition of AGEPC (10(-13) to 10(-9) M) to rat hepatocytes failed to stimulate glucose output, whereas epinephrine (10(-5)M) and glucagon (10(-7)M) stimulated glucose output by 100% or more in these same cells. The effects of AGEPC, epinephrine, vasopressin, and glucagon on glycogen phosphorylase activity and the breakdown of phosphatidylinositol 4,5-bisphosphate were compared in hepatocytes. AGEPC (10(-9)M) promoted the breakdown of phosphatidylinositol 4,5-bisphosphate in a fashion similar to epinephrine (10(-5)M) and vasopressin (10(-7)M). In contrast to the two calcium-mobilizing hormones, epinephrine and vasopressin, AGEPC did not cause an activation of glycogen phosphorylase. Glucagon activation of glycogen phosphorylase was not accompanied by a significant effect on phosphatidylinositol 4,5-bisphosphate hydrolysis. Thus, AGEPC is a chemical mediator which induces the degradation of phosphatidylinositol 4,5-bisphosphate without activating glycogenolysis in hepatocytes.
已在大鼠肝细胞中研究了乙酰甘油醚磷酸胆碱（AGEPC）对糖原分解和磷脂酰肌醇4,5 - 二磷酸的影响。此前，本实验室证明AGEPC可刺激灌注大鼠肝脏的葡萄糖输出，并促进大鼠肝细胞中磷酸肌醇的分解（舒克拉，S.D.，巴克斯顿，D.B.，奥尔森，M.S.，和哈纳汉，D.J.（1983年）《生物化学杂志》258卷，10212 - 10214页）。在本研究中，向大鼠肝细胞中添加AGEPC（10⁻¹³至10⁻⁹M）未能刺激葡萄糖输出，而肾上腺素（10⁻⁵M）和胰高血糖素（10⁻⁷M）在这些相同细胞中可使葡萄糖输出增加100%或更多。在肝细胞中比较了AGEPC、肾上腺素、血管加压素和胰高血糖素对糖原磷酸化酶活性和磷脂酰肌醇4,5 - 二磷酸分解的影响。AGEPC（10⁻⁹M）以类似于肾上腺素（10⁻⁵M）和血管加压素（10⁻⁷M）的方式促进磷脂酰肌醇4,5 - 二磷酸的分解。与两种钙动员激素肾上腺素和血管加压素不同，AGEPC不会引起糖原磷酸化酶的激活。胰高血糖素对糖原磷酸化酶的激活并未伴随对磷脂酰肌醇4,5 - 二磷酸水解的显著影响。因此，AGEPC是一种化学介质，它可诱导磷脂酰肌醇4,5 - 二磷酸的降解而不激活肝细胞中的糖原分解。
