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膳食抗性淀粉与慢性炎症性肠病

Dietary resistant starch and chronic inflammatory bowel diseases.

作者信息

Jacobasch G, Schmiedl D, Kruschewski M, Schmehl K

机构信息

Department of Food Chemistry and Preventive Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke, Bergholz-Rehbrücke.

出版信息

Int J Colorectal Dis. 1999 Nov;14(4-5):201-11. doi: 10.1007/s003840050212.

Abstract

These studies were performed to test the benefit of resistant starch on ulcerative colitis via prebiotic and butyrate effects. Butyrate, propionate, and acetate are produced in the colon of mammals as a result of microbial fermentation of resistant starch and other dietary fibers. Butyrate plays an important role in the colonic mucosal growth and epithelial proliferation. A reduction in the colonic butyrate level induces chronic mucosal atrophy. Short-chain fatty acid enemas increase mucosal generation, crypt length, and DNA content of the colonocytes. They also ameliorate symptoms of ulcerative colitis in human patients and rats injected with trinitrobenzene sulfonic acid (TNBS). Butyrate, and also to a lesser degree propionate, are substrates for the aerobic energy metabolism, and trophic factors of the colonocytes. Adverse butyrate effects occur in normal and neoplastic colonic cells. In normal cells, butyrate induces proliferation at the crypt base, while inhibiting proliferation at the crypt surface. In neoplastic cells, butyrate inhibits DNA synthesis and arrests cell growth in the G1 phase of the cell cycle. The improvement of the TNBS-induced colonic inflammation occurred earlier in the resistant starch (RS)-fed rats than in the RS-free group. This benefit coincided with activation of colonic epithelial cell proliferation and the subsequent restoration of apoptosis. The noncollagenous basement membrane protein laminin was regenerated initially in the RS-fed group, demonstrating what could be a considered lower damage to the intestinal barrier function. The calculation of intestinal short-chain fatty acid absorption confirmed this conclusion. The uptake of short-chain fatty acids in the colon is strongly inhibited in the RS-free group, but only slightly reduced in the animals fed with RS. Additionally, RS enhanced the growth of intestinal bacteria assumed to promote health. Further studies involving patients suffering from ulcerative colitis are necessary to determine the importance of RS in the therapy of a number of intestinal diseases and the maintenance of health.

摘要

进行这些研究是为了通过益生元和丁酸盐效应来测试抗性淀粉对溃疡性结肠炎的益处。丁酸盐、丙酸盐和乙酸盐是哺乳动物结肠中抗性淀粉和其他膳食纤维微生物发酵的产物。丁酸盐在结肠黏膜生长和上皮细胞增殖中起重要作用。结肠丁酸盐水平降低会导致慢性黏膜萎缩。短链脂肪酸灌肠可增加结肠黏膜生成、隐窝长度和结肠细胞的DNA含量。它们还可改善溃疡性结肠炎患者和注射三硝基苯磺酸(TNBS)的大鼠的症状。丁酸盐以及程度较轻的丙酸盐是结肠细胞有氧能量代谢的底物和营养因子。丁酸盐在正常和肿瘤性结肠细胞中都会产生不良影响。在正常细胞中,丁酸盐诱导隐窝底部的增殖,同时抑制隐窝表面的增殖。在肿瘤细胞中,丁酸盐抑制DNA合成并使细胞生长停滞在细胞周期的G1期。在喂食抗性淀粉(RS)的大鼠中,TNBS诱导的结肠炎症改善比无RS组更早出现。这种益处与结肠上皮细胞增殖的激活以及随后凋亡的恢复相一致。非胶原性基底膜蛋白层粘连蛋白最初在RS喂养组中再生,表明对肠道屏障功能的损伤可能较小。肠道短链脂肪酸吸收的计算证实了这一结论。在无RS组中,结肠对短链脂肪酸的摄取受到强烈抑制,但在喂食RS的动物中仅略有减少。此外,RS促进了假定有益健康的肠道细菌的生长。有必要对溃疡性结肠炎患者进行进一步研究,以确定RS在多种肠道疾病治疗和健康维持中的重要性。

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