Lysophosphatidylcholine increases the secretion of cholesteryl ester-poor triacylglycerol-rich lipoproteins by CaCo-2 cells.

To address the effect of lysophosphatidylcholine on triacylglycerol transport in intestine, CaCo-2 cells, grown on semipermeable supports, were incubated with lysophosphatidylcholine solubilized in 1 mM taurocholate. [14C]Palmitoyllysophosphatidylcholine was readily taken up and incorporated predominantly into cellular phospholipids, particularly phosphatidylcholine. Twenty-five percent of the label was found in triacylglycerols. Compared with labelled cellular phospholipids, labelled triacylglycerols were preferentially secreted. Lysophosphatidylcholine caused a profound decrease in cholesteryl ester synthesis and secretion, whereas cellular triacylglycerol mass and triacylglycerol synthesis and secretion were increased. The effect was more pronounced with oleoyllysophosphatidylcholine than with either palmitoyl- or stearyl-lysophosphatidylcholine. Lysophosphatidylcholine increased the secretion of immunoreactive and newly-synthesized apoprotein B (apoB) without altering the rate of apoB synthesis. Thus, luminal lysophosphatidylcholine and/or its uptake decreases cholesterol esterification and secretion, but increases triacylglycerol synthesis and secretion, triacylglycerol mass accumulation and the secretion of apoB by CaCo-2 cells.