INHIBITION OF SHORT-CHAIN FATTY-ACID ABSORPTION AND NA+ ABSORPTION DURING ACUTE COLITIS IN THE RABBIT

INHIBITION OF SHORT-CHAIN FATTY-ACID ABSORPTION AND NA+ ABSORPTION DURING ACUTE COLITIS IN THE RABBIT
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DOI:
10.1016/0016-5085(94)90009-4
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发表时间:
1994-05-01
期刊:
影响因子:
29.4
通讯作者:
DALAL, V
DALAL, V
中科院分区:
医学1区
文献类型:
--
作者:
BUTZNER, JD;MEDDINGS, JB;DALAL, V

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背景/目的:短链脂肪酸为结肠细胞提供能量,促进结肠液和电解质的吸收。研究急性结肠炎对SCFA刺激的Na+吸收和SCFA吸收的影响。方法:将感染小肠结肠炎耶尔森菌的兔近端结肠安装在Ussing小室中,检测基础期间和SCFA、丁酸盐或丙酸刺激后的Na+转运、短路电流和组织电导。结果:在对照组和配对喂养组中,丁酸盐和丙酸促进了基础水平以上的Na+的电中和吸收,表现为粘膜到浆膜和净Na+通量显著增加,而浆膜到粘膜的通量、短路电流或电导没有改变。Na+-H+交换抑制剂阿米洛利可阻断丁酸刺激的Na+吸收和丙酸吸收。在感染组,丁酸和丙酸均不能刺激基础水平以上的结肠Na+吸收。丙酸吸收受到抑制,肾上腺素不能刺激Na+或丙酸吸收。结论:抑制SCFA刺激的Na+-H+交换和SCFA吸收是导致急性结肠炎腹水丢失的原因之一,并可能减少结肠细胞的能量供应。
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 withYersinia 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 concentrations 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.