Effect of synthetic diets on gastrointestinal mucosal DNA synthesis in rats.
Effect of synthetic diets on gastrointestinal mucosal DNA synthesis in rats.
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合成饮食对大鼠胃肠粘膜 DNA 合成的影响。
DOI：
10.1152/ajpgi.1983.244.3.g327
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Lichtenberger,LM
中科院分区：
文献类型：
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作者：
Sircar,B;Johnson,LR;Lichtenberger,LM
伦纳德·比西·西尔卡作者声明：John M.利滕贝格。合成饲料对大鼠胃肠道粘膜DNA合成的影响。Am. J. Physiol.244（Gastrointest.肝脏生理学7）：G327-G335，1983年。等热量的各种合成的液体和固体饮食喂养大鼠在一个LO天的时间内导致一个显着的两到四倍减少胃和结肠粘膜DNA合成相比，饲料喂养的控制。相比之下，小肠增殖活性不受这些市售饮食的影响。这种饮食诱导的粘膜DNA合成减少似乎与食物中蛋白质或脂肪含量的变化无关。在低纤维饲料中添加纤维素后，经过10天的喂养期，结肠粘膜DNA合成量有了小而显著的增加。在随后的实验中，确定在动物食用合成饮食仅1天后，胃和结肠DNA合成的最大减少发生。此外，在进食合成饲料的大鼠中，通常在进食普通饲料后12-16小时发生的泌酸和结肠粘膜DNA合成的急性爆发几乎不存在。这种急性生长反应喂养的情况下不能归因于低于正常含量的铁或纤维在这些饮食中，因为补充这两个因素的水平高于那些在食物中发现未能增加粘膜DNA合成。考虑到营养激素胃泌素作为这种饮食诱导的胃肠道粘膜DNA合成减少的介体的可能重要性，因为最近的研究结果表明，当大鼠喂食合成饮食时，血液胃泌素的正常水平不能维持。泌酸腺;结肠;胃泌素众所周知，胃肠道细胞的生长对饮食控制极其敏感。禁食导致小肠，胃和结肠（1，2，7，11-13，18，24，25）粘膜生长的一般抑郁症。再喂食后，在各种受试动物种属的小肠（2，12，13）、胃（13，35）和结肠粘膜（11，30，31）中，有丝分裂活性和隐窝细胞结构均增加。禁食期间隐窝中细胞生成减少似乎与细胞周期延长有关，这最有可能归因于G1期延迟（11）。再喂食后不久，胃肠道粘膜的大部分细胞同步进入细胞周期的S期。在胃肠道的不同粘膜区域，进食与DNA合成峰值之间的滞后时间从16小时到24小时不等（1，11，13）。目前尚不清楚是什么介导了胃肠道中食物刺激的DNA合成。几个方面-
SIRCAR, BITHI, LEONARD R. JOHNSON, AND LENARD M. LICHTENBERGER. Effect of synthetic diets on gastrointestinal mucosal DNA synthesis in rats. Am. J. Physiol. 244 (Gastrointest. Liver Physiol. 7): G327-G335, 1983.-Isocaloric amounts of a variety of synthetic liquid and solid diets fed to rats over a lo-day period resulted in a significant two-to fourfold decrease in gastric and colonic mucosal DNA synthesis in comparison with chow-fed controls. In contrast, small intestinal proliferative activity was uninfluenced by these commercially available diets. This diet-induced decrease in mucosal DNA synthesis did not appear to be associated with variations in the protein or fat content of the food. Addition of ar-cellulose to these lowfiber diets induced a small but significant increase in colonic mucosal DNA synthesis after a lo-day feeding period. In subsequent experiments, it was determined that the maximal decrease in gastric and colonic DNA synthesis occurred after the animals ate synthetic diets for only 1 day. In addition, the acute burst in oxyntic and colonic mucosal DNA synthesis that normally occurs 12-16 h after the consumption of a chow meal was all but absent in rats eating synthetic diets. The absence of this acute growth response to feeding could not be attributed to the lower-than-normal content of either iron or fiber in these diets because supplementation of both factors to levels higher than those found in chow failed to increase mucosal DNA synthesis. The possible importance of the trophic hormone gastrin as a mediator of this diet-induced decrease in gastrointestinal mucosal DNA synthesis was considered because recent findings suggest that normal levels of blood gastrin are not maintained when rats are fed synthetic diets. oxyntic gland; colon; gastrinGASTROINTESTINAL CELL GROWTH is known to be extremely sensitive to dietary manipulation. Fasting causes general depression of mucosal growth in the small intestine, stomach, and colon (1, 2, 7, 11-13, 18, 24, 25). After refeeding, there is an increase in both mitotic activity and crypt cellularity in the small intestinal (2, 12, 13), gastric (13, 35), and colonic mucosa (11, 30, 31) of various animal species tested. Decreased cell production in the crypt during fasting appears to be related to prolongation of the cell cycle, which is most likely attributable to a delay in the G1 phase (11). Shortly after refeeding, a large percentage of cells of the gastrointestinal mucosa synchronously enter into the S phase of the cell cycle. The lag time between feeding and the peak rate of DNA synthesis varies from 16 to 24 h in the different mucosal regions of the gastrointestinal tract (1, 11, 13). It is presently unclear what mediates the food-stimulated DNA synthesis in the gastrointestinal tract. Several fac-