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大鼠小肠黏膜胆固醇的稳态

Homeostasis of mucosal cholesterol in the small intestine of the rat.

作者信息

Blumer A, Watt S M, Simmonds W J

出版信息

Lipids. 1984 Oct;19(10):721-7. doi: 10.1007/BF02534465.

DOI:10.1007/BF02534465
PMID:6503619
Abstract

This study was undertaken to investigate the capacity of the intestinal mucosa to maintain a constant cholesterol content under conditions where mucosal uptake or cholesterol transport into the lymph were manipulated. Two series of bile-diverted unanaesthetised rats were infused intraduodenally with saline, triolein emulsified with Pluronic F68, or taurocholate with or without added tomatine. Pluronic F68 is a nontoxic detergent which promotes mucosal uptake of polar lipids but not cholesterol. Tomatine is a cholesterol-binding saponin. One series of rats was used for measuring mucosal cholesterol content, DNA and protein after the test infusions. A second series of rats had the thoracic lymph duct cannulated but otherwise remained the same as the first series. The second series was used for measuring the effect of the different infusions on mass cholesterol output into lymph. Mucosal cholesterol content of rats that were not fed decreased with bile-diversion and was restored with taurocholate infusion. This suggested a contribution of luminal cholesterol to the mucosal cholesterol pool. However, evidence for a contribution from the lumen was provided by only one of two groups of rats given infusions which did not promote mucosal uptake of cholesterol. First, addition of tomatine to the taurocholate infusate prevented both the increase in lymph output of cholesterol and the increased mucosal cholesterol content shown in rats given taurocholate alone. Second, in another group of rats in which mucosal uptake of cholesterol was prevented, i.e. in rats given Pluronic F68-triolein emulsions, the increased fat absorption was accompanied by a marked increase in cholesterol output into lymph without a concomitant decrease in mucosal cholesterol content.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在探讨在黏膜摄取或胆固醇转运至淋巴的过程受到操控的条件下,肠黏膜维持恒定胆固醇含量的能力。将两组胆汁分流的未麻醉大鼠经十二指肠内注入生理盐水、用普朗尼克F68乳化的三油酸甘油酯,或添加或不添加番茄碱的牛磺胆酸盐。普朗尼克F68是一种无毒去污剂,可促进极性脂质的黏膜摄取,但不促进胆固醇摄取。番茄碱是一种胆固醇结合皂苷。一组大鼠用于在试验性输注后测量黏膜胆固醇含量、DNA和蛋白质。另一组大鼠进行胸导管插管,其他方面与第一组相同。该组用于测量不同输注对淋巴中胆固醇输出量的影响。未进食大鼠的黏膜胆固醇含量随胆汁分流而降低,经牛磺胆酸盐输注后恢复。这表明肠腔胆固醇对黏膜胆固醇池有贡献。然而,在两组接受不促进胆固醇黏膜摄取的输注的大鼠中,只有一组提供了来自肠腔贡献的证据。首先,在牛磺胆酸盐输注液中添加番茄碱可防止胆固醇淋巴输出增加以及单独给予牛磺胆酸盐的大鼠中出现的黏膜胆固醇含量增加。其次,在另一组阻止胆固醇黏膜摄取的大鼠中,即给予普朗尼克F68 - 三油酸甘油酯乳剂的大鼠中,脂肪吸收增加伴随着淋巴中胆固醇输出显著增加,而黏膜胆固醇含量并未相应降低。(摘要截断于250字)

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本文引用的文献

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