Zarling E J, Mobarhan S
J Lab Clin Med. 1987 May;109(5):556-9.
The effects of malnutrition on the gastrointestinal tract have been previously investigated in animal models using dietary protein restriction. Because malnutrition is clinically a consequence of reduced dietary intake of all macronutrients, we investigated the effect of restricting a balanced diet on intestinal disaccharidases and histologic conditions of rats. Our diet-restricted animals gained less weight (13 +/- 9 gm) than the control animals (158 +/- 27 gm) over the 5-week study. The proximal, middle, and distal small intestinal segments from the experimental animals had reduced mucosal protein content (15 +/- 4 mg vs. 24 +/- 7 mg). In these segments the total amount of maltase was slightly decreased, whereas sucrase and lactase activities were normal or increased. The intestinal villus/crypt ratios were similar in the experimental and control animals. Mucosal cell height was significantly reduced in the diet-restricted groups; however, cell width was normal. We conclude that severely diet-restricted animals have mucosal protein loss caused in part by reduced cell height, but that the disaccharidase enzyme activities are normal. Diet-restricted animals appear to have sufficient intestinal enzymes to support a normal amount of disaccharide hydrolysis.
此前曾在动物模型中利用限制饮食蛋白质的方法研究营养不良对胃肠道的影响。由于临床上营养不良是所有常量营养素饮食摄入量减少的结果，我们研究了限制均衡饮食对大鼠肠道双糖酶和组织学状况的影响。在为期5周的研究中，饮食受限的动物体重增加量（13±9克）低于对照动物（158±27克）。实验动物的近端、中端和远端小肠段的黏膜蛋白含量降低（15±4毫克对24±7毫克）。在这些肠段中，麦芽糖酶总量略有下降，而蔗糖酶和乳糖酶活性正常或升高。实验动物和对照动物的肠绒毛/隐窝比值相似。饮食受限组的黏膜细胞高度显著降低；然而，细胞宽度正常。我们得出结论，严重饮食受限的动物存在黏膜蛋白流失，部分原因是细胞高度降低，但双糖酶活性正常。饮食受限的动物似乎有足够的肠道酶来支持正常量的双糖水解。
