Digestion of triglyceride in the intestine results in the production of 2-monoglyceride and fatty acid. Phosphatidylcholine is hydrolyzed in the lumen to form lysophosphatidylcholine before its absorption. These digestion products are absorbed by the enterocytes through simple diffusion. In contrast, cholesterol absorption seems specific and is energy dependent. After entry into the enterocytes, these lipid digestion products migrate to the endoplasmic reticulum. Both fatty acid-binding protein and sterol carrier protein may be involved in the intracellular transport of fatty acid and cholesterol, respectively. Through predominantly the monoglyceride pathway, monoglycerides and fatty acids are resynthesized to form triglyceride in the endoplasmic reticulum. The lipid droplets, coated with cholesterol, phospholipid, and apolipoproteins, are then further processed in the Golgi apparatus before being released by the enterocytes through exocytosis. As yet, little is known of the factors regulating the formation and release of these chylomicrons by the enterocytes. Although apolipoprotein B is a prerequisite for the formation of chylomicrons, the question of whether its supply is rate limiting for chylomicron formation remains to be demonstrated. Other factors that may play a role in chylomicron formation are luminal phospholipid supply, Ca2+, and microtubules. Chylomicrons and very low-density lipoproteins are probably produced by the enterocytes via different pathways. For example, Pluronic L-81, a hydrophobic surfactant, affects only chylomicron formation and has little effect on very low-density lipoprotein production. The movement of chylomicrons from the intercellular space through the basement membrane to the lamina propria is not fully understood. Once inside the lamina propria, the movement of chylomicrons is probably by diffusion and is greatly facilitated by interstitial hydration; thus the lymphogogic effect of fat absorption may serve an important function for the transfer of chylomicrons from the enterocytes to the lacteal.

To test the regulatory effect of dietary triglyceride (TG) on rat lymphatic apolipoprotein B (apo B) transport, lymph-fistula rats were infused intraduodenally for 8 h at 3 ml/h with a lipid emulsion containing 40 mumol TG labeled with glycerol [9,10-3H(N)]triolein, 7.8 mumol egg phosphatidylcholine, and 57 mumol sodium taurocholate in phosphate-buffered saline with or without 1 mg/h Pluronic L81 (L81). L81 is known to prevent lipid transport in the intestine by inhibiting the formation of chylomicrons (CM). This action of L81 is quickly reversible by merely replacing L81 infusion by saline infusion. In the control rats (without L81 added to the infusate), the amount of apo B secreted in either whole lymph, CM, or the very-low-density lipoprotein (VLDL) fractions did not change significantly during lipid infusion compared with fasting. Compared with the fasting, the apo B output in lymph during L81 plus lipid or saline infusion in the experimental rats did not change significantly. The lymphatic apo B output data were also supported by the incorporation studies using [3H]leucine. In summary, these data demonstrate that the absorption of a physiological load of lipid into lymph does not affect the apo B synthesis in the mucosa or the secretion of apo B in lymph. Furthermore, the action of L81 is probably not by inhibiting intestinal apo B production because apo B secretion was not affected by the presence of L81. This study also demonstrates that the number of CM particles made by the small intestine remains relatively constant during fasting or active lipid uptake and transport. During active lipid absorption, instead of increasing the number of CM, the enterocytes expand the size of the CM particles. Lastly, the number and TG content of VLDL particles synthesized and secreted by the small intestine also seems to remain relatively constant during fasting and active lipid absorption.

The effects of hydrolytic products of carbohydrate, protein, and lipid digestion on jejunal mucosal injury and restitution were assessed in anesthetized rats. Mucosal epithelial integrity was continuously monitored by measuring the blood-to-lumen clearance of 51Cr-labeled EDTA. Perfusion of the lumen with hydrolyzed casein (3%) or glucose (150 mM) did not affect 51Cr-EDTA clearance compared with saline controls. By contrast, perfusion with emulsified lipids (20 mM sodium taurocholate and 10-40 mM oleic acid) increased 51Cr-EDTA clearance in a dose-dependent manner. The lipid-induced increase in 51Cr-EDTA clearance returned toward control levels when the lipid infusion was terminated and saline perfusion resumed. Histological evaluation of jejunal mucosa indicated that the epithelial lining of the villous tips was damaged during lipid infusion and that restitution of the lining occurred within 50 min after resumption of saline perfusion. In vitro studies indicated that neither glucose nor hydrolyzed casein affected the integrity of rat intestinal epithelial cell (IEC-18) monolayers in culture. Oleic acid emulsified in rat hepatic bile produced a dose-dependent disruption of the epithelial monolayer. Biochemical determination of lipid peroxidation products in vivo and in vitro yielded negative results, indicating that the lipid-induced epithelial cell injury was not due to lipid peroxidation. Because the concentrations of the various nutrients used in the present study are similar to those measured in postprandial chyme, the findings of the present study suggest that the intestinal epithelium is injured and restitutes during the normal course of digestion and absorption of a meal.