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溃疡性结肠炎患者粪便对大鼠结肠细胞中丁酸盐氧化的影响。

Influence of feces from patients with ulcerative colitis on butyrate oxidation in rat colonocytes.

作者信息

Jørgensen J R, Mortensen P B

机构信息

Department of Medicine, Copenhagen University Hospital, The Rigshospital, Denmark.

出版信息

Dig Dis Sci. 1999 Oct;44(10):2099-109. doi: 10.1023/a:1026642923168.

Abstract

An impaired oxidation of butyrate has been suggested as a causative factor of ulcerative colitis and, moreover, agents present in colonic luminal contents impair butyrate oxidation in both rat and human colonocytes. To evaluate the overall effect of feces on the production of CO2 and ketone bodies from butyrate oxidation in rat colonocytes, fecal homogenates from 10 healthy subjects and 10 patients with quiescent and 10 patients with active ulcerative colitis were sterile filtrated and added to rat colonocytes incubated with 2, 4, and 10 mmol/liter of stock butyrate, respectively. Addition of fecal filtrate from healthy subjects and patients with quiescent and active ulcerative colitis to colonocytes incubated with 2, 4, and 10 mmol/liter of stock butyrate, respectively, tended to decrease the production of CO2 from butyrate oxidation, whereas ketogenesis was unaffected. The decrease in CO2 production was not explained by the simultaneous addition of fecal short-chain fatty acids (SCFAs). However, a difference in the ability to decrease CO2 production was not found between filtrates from healthy subjects and patients with quiescent and active ulcerative colitis. In conclusion, feces from healthy subjects and patients with quiescent and active ulcerative colitis contain inhibitor(s) of the production of CO2 from butyrate oxidation in colonocytes. However, a specific inhibitory effect of feces from patients with ulcerative colitis on the production of CO2 could not be identified.

摘要

丁酸氧化受损被认为是溃疡性结肠炎的一个致病因素,此外,结肠腔内容物中的物质会损害大鼠和人类结肠细胞中的丁酸氧化。为了评估粪便对大鼠结肠细胞中丁酸氧化产生二氧化碳和酮体的总体影响,对10名健康受试者、10名静止期溃疡性结肠炎患者和10名活动期溃疡性结肠炎患者的粪便匀浆进行无菌过滤,并分别添加到与2、4和10 mmol/L储备丁酸孵育的大鼠结肠细胞中。分别将健康受试者、静止期和活动期溃疡性结肠炎患者的粪便滤液添加到与2、4和10 mmol/L储备丁酸孵育的结肠细胞中,往往会降低丁酸氧化产生的二氧化碳量,而酮生成不受影响。同时添加粪便短链脂肪酸(SCFA)并不能解释二氧化碳产生量的减少。然而,在健康受试者以及静止期和活动期溃疡性结肠炎患者的滤液之间,未发现降低二氧化碳产生能力的差异。总之,健康受试者以及静止期和活动期溃疡性结肠炎患者的粪便中含有结肠细胞中丁酸氧化产生二氧化碳的抑制剂。然而,无法确定溃疡性结肠炎患者粪便对二氧化碳产生的特异性抑制作用。

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