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饥饿的结肠——黏膜营养减少、吸收减少与结肠炎。

The starved colon--diminished mucosal nutrition, diminished absorption, and colitis.

作者信息

Roediger W E

机构信息

Department of Surgery, Queen Elizabeth Hospital, Woodville, Australia.

出版信息

Dis Colon Rectum. 1990 Oct;33(10):858-62. doi: 10.1007/BF02051922.

Abstract

Nutrition of colonic epithelial cells is mainly from short chain fatty acids (SCFAs) produced by bacterial fermentation in the colonic lumen. n-Butyrate contributes more carbon of oxidation to epithelial cells than glucose or glutamine from the vasculature. Incomplete starvation of colonic epithelial cells through lack of luminal SCFAs leads, in the short term, to mucosal hypoplasia with either diminished absorption or diarrhea. A chronic lack of SCFAs or complete organ starvation in conjunction with other factors leads to nutritional colitis, either "diversion colitis" or "starvation colitis." Whether predominantly diarrhea or colitis develops in mucosal malnutrition appears to depend upon the severity and duration of starvation. Ulcerative colitis may be classified as a nutritional colitis in that colonic epithelial cells are unable to utilize SCFAs reflecting epithelial starvation despite abundant SCFAs.

摘要

结肠上皮细胞的营养主要来自结肠腔内细菌发酵产生的短链脂肪酸(SCFAs)。与来自血管的葡萄糖或谷氨酰胺相比,正丁酸盐为上皮细胞提供更多的氧化碳。由于缺乏腔内SCFAs导致结肠上皮细胞不完全饥饿,短期内会导致黏膜发育不全,伴有吸收减少或腹泻。长期缺乏SCFAs或与其他因素一起导致的完全器官饥饿会导致营养性结肠炎,即“改道性结肠炎”或“饥饿性结肠炎”。黏膜营养不良时主要出现腹泻还是结肠炎似乎取决于饥饿的严重程度和持续时间。溃疡性结肠炎可归类为营养性结肠炎,因为尽管有大量SCFAs,但结肠上皮细胞无法利用它们,这反映了上皮细胞饥饿。

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