Kvietys P R, Specian R D, Grisham M B, Tso P
Department of Physiology, Louisiana State University Medical Center, Shreveport 71130.
Am J Physiol. 1991 Sep;261(3 Pt 1):G384-91. doi: 10.1152/ajpgi.1991.261.3.G384.
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.
在麻醉大鼠中评估了碳水化合物、蛋白质和脂质消化的水解产物对空肠黏膜损伤和修复的影响。通过测量51Cr标记的EDTA从血液到肠腔的清除率来持续监测黏膜上皮的完整性。与生理盐水对照组相比,用水解酪蛋白(3%)或葡萄糖(150 mM)灌注肠腔对51Cr-EDTA清除率没有影响。相比之下,用乳化脂质(20 mM牛磺胆酸钠和10 - 40 mM油酸)灌注以剂量依赖的方式增加了51Cr-EDTA清除率。当终止脂质灌注并恢复生理盐水灌注时,脂质诱导的51Cr-EDTA清除率增加恢复到对照水平。空肠黏膜的组织学评估表明,在脂质灌注期间绒毛尖端的上皮内衬受损,并且在恢复生理盐水灌注后50分钟内发生了内衬修复。体外研究表明,葡萄糖和水解酪蛋白均不影响培养的大鼠肠上皮细胞(IEC-18)单层的完整性。大鼠肝胆汁中乳化的油酸对上皮单层产生剂量依赖性破坏。体内和体外脂质过氧化产物的生化测定结果均为阴性,表明脂质诱导的上皮细胞损伤不是由于脂质过氧化。由于本研究中使用的各种营养素的浓度与餐后食糜中测量的浓度相似,本研究结果表明,在一餐的正常消化和吸收过程中,肠上皮会受到损伤并进行修复。