JEJUNAL MUCOSAL INJURY AND RESTITUTION - ROLE OF HYDROLYTIC PRODUCTS OF FOOD DIGESTION
JEJUNAL MUCOSAL INJURY AND RESTITUTION - ROLE OF HYDROLYTIC PRODUCTS OF FOOD DIGESTION
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DOI：
10.1152/ajpgi.1991.261.3.g384
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发表时间：
1991-09-01
影响因子：
--
通讯作者：
TSO, P
中科院分区：
文献类型：
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作者：
KVIETYS, PR;SPECIAN, RD;TSO, P
在麻醉大鼠中评估碳水化合物、蛋白质和脂质消化的水解产物对空肠粘膜损伤和恢复的影响。 通过测量Cr-51标记的EDTA的血液-管腔清除率连续监测粘液上皮完整性。 与生理盐水对照相比，用水解酪蛋白（3%）或葡萄糖（150 mM）灌注管腔不影响Cr-51-EDTA清除率。 相比之下，灌注乳化脂质（20 mM牛磺胆酸钠和10-40 mM油酸）增加Cr-51-EDTA清除率的剂量依赖性方式。 当终止脂质输注并恢复生理盐水灌注时，脂质诱导的Cr-51-EDTA清除率增加恢复至对照水平。 空肠粘膜的组织学评价表明，绒毛尖端的上皮衬里在脂质灌注过程中受损，恢复盐水灌注后50分钟内发生的衬里。 体外研究表明，无论是葡萄糖还是水解酪蛋白都不会影响培养的大鼠肠上皮细胞（IEC-18）单层的完整性。 油酸乳化在大鼠肝胆汁中产生了剂量依赖性破坏的上皮细胞单层。 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，因此本研究的结果表明，在正常的消化和吸收过程中，肠上皮细胞受到损伤并恢复。
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 Cr-51-labeled EDTA. Perfusion of the lumen with hydrolyzed casein (3%) or glucose (150 mM) did not affect Cr-51-EDTA clearance compared with saline controls. By contrast, perfusion with emulsified lipids (20 mM sodium taurocholate and 10-40 mM oleic acid) increased Cr-51-EDTA clearance in a dose-dependent manner. The lipid-induced increase in Cr-51-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.