Tijburg L B, Houweling M, Geelen M J, Van Golde L M
Laboratory of Veterinary Biochemistry, University of Utrecht, The Netherlands.
Biochem J. 1989 Feb 1;257(3):645-50. doi: 10.1042/bj2570645.
Exposure of isolated rat hepatocytes to glucagon or chlorophenylthio cyclic AMP led to an inhibition of the incorporation of [1,2-14C]ethanolamine into phosphatidylethanolamine. Pulse-chase experiments and measurement of the activities of the enzymes involved in the CDP-ethanolamine pathway provided evidence that the inhibitory effect of glucagon on the synthesis de novo of phosphatidylethanolamine was not caused by a diminished conversion of ethanolamine phosphate into CDP-ethanolamine. The observations suggested that the glucagon-induced inhibition of the biosynthesis of phosphatidylethanolamine is probably due to a decreased supply of diacylglycerols, resulting in a decreased formation of phosphatidylethanolamine from CDP-ethanolamine and diacylglycerols.
将分离的大鼠肝细胞暴露于胰高血糖素或氯苯硫基环磷酸腺苷会导致[1,2-14C]乙醇胺掺入磷脂酰乙醇胺受到抑制。脉冲追踪实验以及对参与CDP-乙醇胺途径的酶活性的测量提供了证据，表明胰高血糖素对磷脂酰乙醇胺从头合成的抑制作用并非由磷酸乙醇胺向CDP-乙醇胺的转化减少所致。这些观察结果表明，胰高血糖素诱导的磷脂酰乙醇胺生物合成抑制可能是由于二酰基甘油供应减少，导致由CDP-乙醇胺和二酰基甘油形成的磷脂酰乙醇胺减少。
