Jejunal Mucosal Injury and Restitution: Role of Hydrolytic Products of Food Digestion P. R. KVIETYS,R. D. SPECIAN,M. B. GRISHAM,AND P. TSO American Journal of Physiology 24:G384-G391,1991

Abstract

The authors examined the effects of hydrolytic products of carbohydrate, protein, and lipid digestion on jejunal injury and restitution in anesthetized rats. Mucosal epithelial integrity was assessed by measuring blood-to-lumen clearance of ⁵¹Cr-labeled EDTA administered as a bolus into the femoral vein. When the intestinal lumen was perfused with 3% hydrolyzed casein or 150 mmol/L glucose there was no effect on ⁵¹Cr-EDTA clearance when compared with saline controls. However, perfusion with emulsified lipids (20 mmol/L sodium taurocholate and 10 to 40 mmol/L oleic acid) resulted in a statistically significant (p < .05) increase in ⁵¹Cr-EDTA clearance in a dose-dependent fashion. When lipid infusion was terminated and saline perfusion resumed, ⁵¹Cr-EDTA clearance returned to control levels.

Histologic examination of the jejunal mucosa revealed damage of the epithelial lining of the villous tips in animals treated with lipid infusion. The injury was characterized by gaps in the epithelial lining of the villous tips and the presence of exfoliated cells in the mucous layer overlying the disrupted epithelium. After termination of the lipid infusion, epithelial integrity was reestablished within 50 minutes. Nearly 50% of the villi show a discontinuous epithelium at their tips immediately after lipid perfusion is terminated. Subsequent perfusion with saline results in partial restitution with only 14% of the villi affected 30 minutes and 2.6% 50 minutes later.

In vitro studies using monolayer cultures of a rat intestinal epithelial cell line (IEC-18) demonstrated that neither glucose nor hydrolyzed casein had a deleterious effect on cell integrity. However, oleic acid emulsified in rat hepatic bile produced a dose-dependent disruption of the epithelial cell monolayer when added to the cultures.

Biochemical determinations of lipid peroxidation products both in vivo and in vitro did not reveal any significant differences among the various groups, suggesting that the lipid-induced injury was not due to lipid peroxidation.

The authors conclude that because the concentrations of the various nutrients used in the present study are similar to those found in postprandial chyme, their findings suggest that intestinal epithelial injury and restitution take place during the course of digestion and absorption of a meal.