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大鼠乳糜微粒残余胆固醇的胆汁排泄:对其血浆池扩张的反应及胆汁酸合成受刺激的促进作用

Biliary excretion of chylomicron remnant cholesterol in the rat: responses to the expansion of their plasma pool and promoting role of stimulated bile-acid synthesis.

作者信息

Carrella M, Csillaghy A, de Mercato R, D'Arienzo A

机构信息

Cattedra di Gastroenterologia, Facoltà di Medicina e Chirurgia, Università degli Studi di Udine, Italy.

出版信息

Clin Sci (Lond). 1995 Aug;89(2):121-8. doi: 10.1042/cs0890121.

Abstract
  1. Chylomicron remnants, the intermediate intestinal lipoproteins carrying the bulk of dietary cholesterol, are actively taken up and degraded in the hepatocytes, releasing cholesterol which can be excreted in bile. To study this pathway, a mass of remnants, leading to a consistent rise in hepatic cholesterol, was administered as an intravenous bolus in rats with chronic bile fistula equilibrated by water, electrolyte and taurocholate infusions, and changes in biliary lipids and bile acids were evaluated for up to 24 h in comparison with baseline. 2. A mean 16% increase in the net output of bile acids was observed at each time interval after lipoprotein injection, accounting for a 24h cumulative excretion of approximately one-third of the administered cholesterol mass. These changes did not reach statistical significance however. The cholesterol output and concentrations of all biliary lipids did not vary either. Without taurocholate replacement, remnants injection was followed by a 15-20% decrease in bile acid and bile lipid secretion, presumably due to an insufficient hepatic bile-acid flux. 3. When [3H]cholesterol-labelled remnants were administered at the same mass in the chronic equilibrated bile fistula model, 21% of injected radioactivity was excreted in 24h, distributing mostly in acidic rather than neutral sterols (20.02 +/- 1.85 compared with 1.07 +/- 0.04), with an acidic to neutral sterol mean ratio of 16. 4. To exclude interfering effects from the administered cholesterol mass and chronic bile fistula, 3H-labelled remnants were also studied as a cholesterol trace injected in rats with acute bile fistula.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 乳糜微粒残粒是携带大部分膳食胆固醇的肠道中间脂蛋白,在肝细胞中被积极摄取并降解,释放出的胆固醇可通过胆汁排泄。为研究该途径,将大量导致肝脏胆固醇持续升高的残粒以静脉推注的方式给予经水、电解质和牛磺胆酸盐输注平衡的慢性胆瘘大鼠,并与基线相比,评估长达24小时的胆汁脂质和胆汁酸变化。2. 脂蛋白注射后的每个时间间隔,胆汁酸净输出量平均增加16%,24小时累积排泄量约占所给予胆固醇量的三分之一。然而,这些变化未达到统计学意义。胆固醇输出量和所有胆汁脂质的浓度也没有变化。在不补充牛磺胆酸盐的情况下,注射残粒后胆汁酸和胆汁脂质分泌减少15 - 20%,可能是由于肝脏胆汁酸通量不足。3. 在慢性平衡胆瘘模型中以相同量给予[3H]胆固醇标记的残粒时,24小时内21%的注射放射性物质被排泄,主要分布在酸性而非中性固醇中(分别为20.02±1.85和1.07±0.04),酸性与中性固醇的平均比值为16。4. 为排除所给予胆固醇量和慢性胆瘘的干扰作用,还将3H标记的残粒作为胆固醇示踪剂注射到急性胆瘘大鼠中进行研究。(摘要截短于250字)

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