Jambunathan L R, Neuhoff D, Younoszai M K
Am J Clin Nutr. 1981 Sep;34(9):1879-84. doi: 10.1093/ajcn/34.9.1879.
In infants suffering from protein-calorie malnutrition, the decreased intestinal mucosal lactase specific activity could be due either to the protein-calorie malnutrition or to the commonly associated enteritis (viral or bacterial) and intestinal parasites. We studied intestinal mucosal disaccharidase (lactase, sucrase, and maltase) specific activity in suckling (1 and 2 wk old), weanling (3 wk old), and postweaning (4 and 6 wk old) control and growth-retarded (malnourished) rats. Growth retardation was induced by feeding mother rats and postweaning rats a diet deficient in protein. In the malnourished rats, with few exceptions, specific activity of the disaccharidases in the intestinal mucosa were similar to those in the corresponding control groups of rats. However, because of marked mucosal atrophy total intestinal mucosal disaccharidase activities were more than 50% lower in the malnourished rats. These findings suggest that the specific activity of the intestinal mucosal disaccharidases is not affected by malnutrition per se.
在患有蛋白质 - 热量营养不良的婴儿中,肠道黏膜乳糖酶的比活性降低可能是由于蛋白质 - 热量营养不良,或者是由于常见的伴随性肠炎(病毒性或细菌性)及肠道寄生虫。我们研究了哺乳(1周龄和2周龄)、断奶(3周龄)以及断奶后(4周龄和6周龄)的对照大鼠和生长迟缓(营养不良)大鼠的肠道黏膜二糖酶(乳糖酶、蔗糖酶和麦芽糖酶)比活性。通过给母鼠和断奶后的大鼠喂食蛋白质缺乏的饮食来诱导生长迟缓。在营养不良的大鼠中,除了少数例外情况,肠道黏膜中二糖酶的比活性与相应对照组大鼠相似。然而,由于明显的黏膜萎缩,营养不良大鼠的肠道黏膜总二糖酶活性降低了50%以上。这些发现表明,肠道黏膜二糖酶的比活性本身不受营养不良的影响。