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兔急性结肠炎期间短链脂肪酸吸收和Na⁺吸收的抑制作用

Inhibition of short-chain fatty acid absorption and Na+ absorption during acute colitis in the rabbit.

作者信息

Butzner J D, Meddings J B, Dalal V

机构信息

Gastrointestinal Research Group, University of Calgary, Alberta, Canada.

出版信息

Gastroenterology. 1994 May;106(5):1190-8. doi: 10.1016/0016-5085(94)90009-4.

Abstract

BACKGROUND/AIMS: Short-chain fatty acids (SCFAs) provide energy for colonocytes and stimulate colonic fluid and electrolyte absorption. The impact of acute colitis on SCFA-stimulated Na+ absorption and SCFA absorption was examined.

METHODS

Proximal colon from rabbits infected with Yersinia entercolitica, a pair-fed group, and controls was mounted in Ussing chambers, and Na+ transport, short-circuit current, and tissue conductance were examined during a basal period and after stimulation with the SCFAs, butyrate, or propionate. Propionate transport and luminal SCFA concentration were evaluated.

RESULTS

Butyrate and propionate stimulated electroneutral Na+ absorption above basal levels in the control and pair-fed groups, as evidenced by significant increases in mucosal-to-serosal and net Na+ fluxes with no change in serosal-to-mucosal flux, short-circuit current, or conductance. Butyrate-stimulated Na+ absorption and propionate absorption were blocked by amiloride, an inhibitor of Na(+)-H+ exchange. In the infected group, both butyrate and propionate failed to stimulate colonic Na+ absorption above basal levels. Propionate absorption was inhibited, and epinephrine failed to stimulate Na+ or propionate absorption. Luminal SCFA concentrations were increased in acute colitis.

CONCLUSIONS

Inhibition of SCFA-stimulated Na(+)-H+ exchange and SCFA absorption contribute to the diarrheal fluid loses observed in acute colitis and may reduce colonocyte energy supply.

摘要

背景/目的:短链脂肪酸(SCFAs)为结肠细胞提供能量,并刺激结肠液体和电解质吸收。本研究检测了急性结肠炎对SCFAs刺激的Na⁺吸收和SCFAs吸收的影响。

方法

将感染小肠结肠炎耶尔森菌的家兔的近端结肠、一对饲养组家兔的近端结肠以及对照组家兔的近端结肠安装在Ussing chamber中,在基础期以及用SCFAs、丁酸盐或丙酸盐刺激后,检测Na⁺转运、短路电流和组织电导。评估丙酸盐转运和肠腔SCFAs浓度。

结果

在对照组和一对饲养组中,丁酸盐和丙酸盐刺激电中性Na⁺吸收高于基础水平,表现为黏膜到浆膜和净Na⁺通量显著增加,而浆膜到黏膜通量、短路电流或电导无变化。丁酸盐刺激的Na⁺吸收和丙酸盐吸收被Na⁺-H⁺交换抑制剂阿米洛利阻断。在感染组中,丁酸盐和丙酸盐均未能刺激结肠Na⁺吸收高于基础水平。丙酸盐吸收受到抑制,肾上腺素未能刺激Na⁺或丙酸盐吸收。急性结肠炎时肠腔SCFAs浓度升高。

结论

SCFAs刺激的Na⁺-H⁺交换和SCFAs吸收受到抑制,导致急性结肠炎时出现腹泻性液体丢失,并可能减少结肠细胞能量供应。

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