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肠道细菌过度生长在大鼠乙醇生成和代谢中的作用。

Role of intestinal bacterial overgrowth in ethanol production and metabolism in rats.

作者信息

Baraona E, Julkunen R, Tannenbaum L, Lieber C S

出版信息

Gastroenterology. 1986 Jan;90(1):103-10. doi: 10.1016/0016-5085(86)90081-8.

Abstract

To investigate the role of intestinal bacterial overgrowth on the production and metabolism of ethanol, rats with a jejunal self-filling diverticulum (blind-loop) were compared to controls with a self-emptying diverticulum. Both endogenous ethanol and acetaldehyde were found in the blind-loop contents. Intragastric administration of sucrose produced a marked increase in acetaldehyde and acetate in the portal venous blood, with only a modest elevation of ethanol. Blind-loop contents readily oxidized ethanol to acetaldehyde in a concentration-dependent manner and more actively under aerobic than anaerobic conditions. This oxidation was inhibited by antibiotics and was reproduced with isolated microorganisms. Intragastric administration of ethanol to rats with blind-loops markedly increased acetaldehyde and acetate concentrations in the portal vein and, to a lesser extent, in the systemic blood, compared with the controls. By contrast, both portal and systemic blood ethanol concentrations were lower in the rats with a blind-loop compared with controls, even though the amounts of ethanol retained in the digestive tract were similar. A dose of ethanol about twice as large as in controls was required to produce similar systemic blood levels. Both in rats with a blind-loop and in the controls, the areas under the curve of blood ethanol concentrations were smaller after intragastric than after intravenous ethanol administration (1 g ethanol/kg body wt). This difference was exaggerated in the rats with a blind-loop. Thus, a considerable amount of ethanol is oxidized in the gastrointestinal lumen of rats with a blind-loop. The resulting high concentrations of acetaldehyde, both in the intestinal lumen and the portal blood, may have deleterious effects on the gastrointestinal mucosa and the liver.

摘要

为研究肠道细菌过度生长在乙醇生成和代谢中的作用,将患有空肠自充盈憩室(盲袢)的大鼠与具有自排空憩室的对照大鼠进行比较。在盲袢内容物中发现了内源性乙醇和乙醛。胃内给予蔗糖可使门静脉血中乙醛和乙酸盐显著增加,而乙醇仅有适度升高。盲袢内容物能以浓度依赖的方式将乙醇迅速氧化为乙醛,且在有氧条件下比无氧条件下氧化更活跃。这种氧化作用受到抗生素抑制,并可被分离出的微生物重现。与对照组相比,给患有盲袢的大鼠胃内给予乙醇后,门静脉和全身血液中的乙醛和乙酸盐浓度显著增加,全身血液中的增加程度较小。相比之下,尽管消化道中保留的乙醇量相似,但患有盲袢的大鼠门静脉和全身血液中的乙醇浓度均低于对照组。产生相似的全身血液水平所需的乙醇剂量约为对照组的两倍。无论是患有盲袢的大鼠还是对照组,胃内给予乙醇后血乙醇浓度曲线下面积均小于静脉给予乙醇(1 g乙醇/千克体重)后。这种差异在患有盲袢的大鼠中更为明显。因此,患有盲袢的大鼠胃肠道腔内会氧化大量乙醇。肠道腔内和门静脉血中由此产生的高浓度乙醛可能会对胃肠道黏膜和肝脏产生有害影响。

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