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大鼠肝细胞中磷脂酰胆碱分解代谢调节的头部基团特异性

Head group specificity in the regulation of phosphatidylcholine catabolism in rat hepatocytes.

作者信息

Tijburg L B, Vance D E

机构信息

Lipid and Lipoprotein Research Group, University of Alberta, Edmonton, Canada.

出版信息

Biochim Biophys Acta. 1991 Sep 11;1085(2):178-83. doi: 10.1016/0005-2760(91)90092-v.

Abstract

Previous studies have shown that the catabolism of PC is regulated in choline-deficient hepatocytes and the concentration of phosphatidylcholine (PC) might be an important regulatory factor (Tijburg, L.B.M., Nishimaki-Mogami, T. and Vance, D.E. (1991) Biochim. Biophys. Acta, 1085, 167-177). In the present study we investigated the head group specificity of the regulation of PC catabolism. Supplementation of choline-deficient rat hepatocytes, prelabeled with [3H]choline, with dimethylethanolamine increased the catabolism of PC by 1.6-fold after 6 h. This effect was accompanied by a 2.5-fold increase in the production of [3H]glycerophosphocholine (GPC). Radioactivity associated with lysoPC was decreased by 50% in dimethylethanolamine-treated cells. Supplementation of the cells with monomethylethanolamine had little effect on the degradation of PC. In other experiments choline-deficient cells were prelabeled with [3H]methionine. Treatment of the cells with dimethylethanolamine increased the formation of [3H]GPC by 5-fold, while the production of lysoPC was inhibited by 60%. Supplementation of the medium with monomethylethanolamine resulted in a 2-fold increase in labeled GPC, with a concomitant decrease of [3H]lysoPC by approx. 25%. We conclude that the formation of phosphatidyldimethylethanolamine from its corresponding base mimics the effect of the synthesis of PC from choline in increasing PC catabolism, whereas the effect of monomethylethanolamine is much less pronounced.

摘要

先前的研究表明,在胆碱缺乏的肝细胞中,磷脂酰胆碱(PC)的分解代谢受到调节,磷脂酰胆碱(PC)的浓度可能是一个重要的调节因子(Tijburg, L.B.M., Nishimaki-Mogami, T. 和 Vance, D.E. (1991) Biochim. Biophys. Acta, 1085, 167 - 177)。在本研究中,我们研究了PC分解代谢调节的头部基团特异性。用[3H]胆碱预标记的胆碱缺乏大鼠肝细胞补充二甲基乙醇胺后,6小时内PC的分解代谢增加了1.6倍。这种效应伴随着[3H]甘油磷酸胆碱(GPC)产量增加2.5倍。在二甲基乙醇胺处理的细胞中,与溶血磷脂酰胆碱相关的放射性降低了50%。用单甲基乙醇胺补充细胞对PC的降解影响很小。在其他实验中,胆碱缺乏的细胞用[3H]甲硫氨酸预标记。用二甲基乙醇胺处理细胞使[3H]GPC的形成增加了5倍,而溶血磷脂酰胆碱的产生受到60%的抑制。用单甲基乙醇胺补充培养基导致标记的GPC增加2倍,同时[3H]溶血磷脂酰胆碱约减少25%。我们得出结论,由其相应碱基形成磷脂酰二甲基乙醇胺在增加PC分解代谢方面模拟了由胆碱合成PC的效果,而单甲基乙醇胺的效果则不那么明显。

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