Regulation of apolipoprotein secretion by biliary lipids in newborn swine intestinal epithelial cells

Biliary lipids, composed of bile acids, cholesterol, and phosphatidylcholin e, are a major source of luminal lipid in the small intestine. In the prese nt study in a newborn swine intestinal epithelial cell line (IPEC-1), tauro cholate and phosphatidylcholine were found to have no effect on apolipoprot ein B (apo B) secretion but did significantly increase the basolateral secr etion of apo A-I. This regulation of apo A-I secretion occurred at the pret ranslational level for taurocholate and at the posttranslational level for phosphatidylcholine. The regulation of apo A-I secretion by phosphatidylcho line did not involve changes in apo A-I degradation and may involve mobiliz ation of a preformed pool of apo A-I. Cholesterol, whether solubilized with taurocholate or phosphatidylcholine, had no effect on the secretion of eit her apo B or apo A-I. However, when taurocholate, phosphatidylcholine, and cholesterol were combined, apo B secretion was decreased, and the increase in apo A-I secretion noted with taurocholate and phosphatidylcholine alone was ablated. Another primary bile acid, taurochenodeoxycholate, was found t o decrease apo B secretion but had no effect on apo A-I secretion. However, the significance of this effect is uncertain, since this bile acid caused significant cellular membrane injury, as evidenced by increased apical medi um lactate dehydrogenase activity. Phosphatidylcholine, but not taurocholat e, dramatically increased the basolateral secretion of radiolabeled phospho lipid with a modest increase in cellular triglyceride radiolabeling. Furthe rmore, this effect of phosphatidylcholine on lipid synthesis did not requir e significant hydrolysis or uptake of the phosphatidylcholine molecule. Stu dies using radiolabeled taurocholate did not demonstrate active transport o f taurocholate by these cells.