The Effect of Dimethylethanolamine on Hepatic and Biliary Phospholipid Metabolism

Abstract

AIM: To investigate the influence of dimethylethanolamine (DMEA), a phosphatidylcholine (PC) precursor, on hepatic and biliary PC metabolism. METHOD: HepG-2 cells, perfused rat liver and patients with bile fistula were exposed to exogenous DMEA. RESULTS: DMEA added to HepG-2 cell culture caused accumulation of phophatidyldimethylethanolamine (PDMEA) in the cells. In the presence of C14-acetate, the incorporation of C14-fatty acids into PDMEA increased, while incorporation into PC decreased as a function of DMEA concentration in the medium. Incorporation into phosphatidylethanolamine (PEA) and phosphatidylserine (PS) was unaffected. Accumulation of PDMEA in the cells continued to increase for 24 h and was maximal in the presence of 0.2 mM DMEA. The concentration of cellular PDMEA and PC were 20 and 35 nmoles per mg protein, respectively. The fatty acid composition of PDMEA resembled that of PC. PDMEA was converted to PC upon removal of DMEA from the medium. When DMEA was added to the perfused rat liver, PDMEA were detected in bile. In the presence of C14-acetate, the specific radioactivity of PDMEA was 5 to 10 times higher than that of PC. PDMEA of high specific radioactivity was also isolated from liver microsomes. The fatty acid composition of biliary PDMEA resembled that of microsomal PDMEA in contrast to PC which was enriched with 16:0 and 18:2. CONCLUSION: Exogenous DMEA can modulate bile lipid composition in HepG-2 cells and perfused rat liver.