Phospholipid metabolism in rat intestinal mucosa after oral administration of lysophospholipids

The present results indicate that PS, a phospholipid contained in small amounts in the human diet and not included in plasma lipoproteins, may be used to influence phospholipid metabolism in intestinal mucosal cells. Since PS influx into absorptive cells occurs after its hydrolysis to lysoPS, this metabolite may be used to increase the absorption of this phospholipid. These data show that lysoPS, after diffusion into intestinal cells, is sequentially converted into PS and PE (which make up a minor fraction of the lipids present in lipoproteins). As expected, lysoPS given together with radiolabeled unsaturated fatty acids was unable to promote their transfer into plasma lipoproteins. In this respect lysoPS differed from lysoPC, the latter increasing the appearance of dietary fatty acids in plasma. When given together, lysoPS decreased the lysoPC-induced transfer of unsaturated fatty acids into plasma. This effect required addition of triglycerides to the lipid mixture. In attempting to explain this triacylglycerol-dependent inhibition by lysoPS, we found that this phospholipid increased the incorporation of glycerol into mucosal cell PC. In contrast, lysoPC was inhibitory. Furthermore, in the presence of labeled inositol, lysoPC (but not lysoPS) promoted the appearance of labeled phosphatidylinositol. The data thus suggest that the two lysophospholipids differ in promoting the two main pathways of PC synthesis in the intestinal cells. While lysoPC favors PC synthesis by reacylation, lysoPS enhances the CDP-choline pathway of PC synthesis.