Ortega M A, Nunez M C, Gil A, Sánchez-Pozo A
Department of Biochemistry, Faculty of Pharmacy, University of Granada, Spain.
J Nutr. 1995 Jun;125(6):1413-8. doi: 10.1093/jn/125.6.1413.
Previous studies in very young rats have shown that dietary nucleotides improve small intestine repair after injury or malnutrition. To investigate the potential effect of nucleotides in old rats, which have a diminished capability for intestinal repair, 17-mo-old rats were deprived of food for 5 d and then fed a nucleotide-free diet or a nucleotide-supplemented diet for 3 or 6 d. Intestinal jejunal and ileal mucosal weight, protein and DNA were evaluated as intestinal growth markers, and brush-border maltase, sucrase, lactase and aminopeptidase activities were evaluated as intestinal differentiation markers. The adenine nucleotide pool and the adenylate energy charge were also evaluated as indices of nucleotide availability. Food deprivation significantly decreased mucosal growth markers as well as differentiation markers in both jejunum and ileum. The ATP pool was also significantly depressed, but the adenylate energy charge was not significantly altered. To a certain extent, refeeding restored the losses, but in the rats that were fed the nucleotide-free diet, the restoration of the jejunum was significantly slower and the restoration of the ileum differentiation markers was incomplete compared with the rats fed the nucleotide-supplemented diet. The results suggest that dietary nucleotide intake in the elderly may accelerate the normal physiological intestinal response to refeeding after food deprivation.
先前对幼龄大鼠的研究表明,饮食中的核苷酸可促进损伤或营养不良后小肠的修复。为了研究核苷酸对肠道修复能力减弱的老龄大鼠的潜在影响,对17月龄大鼠禁食5天,然后分别给予无核苷酸饮食或补充核苷酸的饮食3天或6天。评估空肠和回肠黏膜重量、蛋白质和DNA作为肠道生长标志物,评估刷状缘麦芽糖酶、蔗糖酶、乳糖酶和氨肽酶活性作为肠道分化标志物。还评估了腺嘌呤核苷酸池和腺苷酸能荷作为核苷酸可用性的指标。禁食显著降低了空肠和回肠的黏膜生长标志物以及分化标志物。ATP池也显著降低,但腺苷酸能荷没有显著改变。在一定程度上,重新喂食可恢复这些损失,但与喂食补充核苷酸饮食的大鼠相比,喂食无核苷酸饮食的大鼠空肠的恢复明显较慢,回肠分化标志物的恢复不完全。结果表明,老年人摄入饮食中的核苷酸可能会加速食物剥夺后正常的肠道再喂养生理反应。