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大豆磷脂酰胆碱诱导的大鼠甘油三酯淋巴吸收增强取决于乳糜微粒的形成。

Soybean phosphatidylcholine-induced enhancement of lymphatic absorption of triglyceride depends on chylomicron formation in rats.

作者信息

Nishimukai Megumi, Hara Hiroshi

机构信息

Creative Research Initiative Sousei, Hokkaido University, Sapporo, Japan.

出版信息

Biosci Biotechnol Biochem. 2007 May;71(5):1192-7. doi: 10.1271/bbb.60654. Epub 2007 May 7.

Abstract

We investigated whether chylomicron formation is involved in the dietary phosphatidylcholine (PC)-induced increase in triglyceride (TG) absorption using an inhibitor of chylomicron formation, pluronic L-81 (L-81). In rats, cannulas were implanted into the duodenum (exps. 1 and 2) and the mesenteric lymph duct (exp. 1), and an emulsified lipid solution containing the test lipids (soybean oil, SO or soybean oil plus phosphatidylcholine, LE) with or without L-81 was infused through a duodenal cannula at a rate 3 ml/h for 2 h, and followed by infusion of a glucose-NaCl solution for 2 h. Mesenteric lymph was collected for 4 h (exp. 1). In exp. 2, the mucosa and contents of the small intestine were collected at 20, 40, or 90 min after the start of duodenal infusion of the test lipid to evaluate accumulation of lipids incorporated into the mucosa in the rats without a lymph cannula. In exp. 1, lymphatic TG outputs rapidly increased with infusion of both test lipids without L-81, but L-81 abolished these increases. TG accumulated in the small intestinal mucosa with L-81 treatment in a time-dependent manner, but the levels of accumulation were similar between the SO and LE groups (exp. 2). There were no differences in the amounts of lipid remaining in the small intestinal lumen between the L-81-treated SO and LE groups. These results indicate that uptake of lipid into the mucosal cells was not increased by LE. We conclude that the formation of chylomicron is responsible for increases in the promotive effect of a high level of dietary PC on the lymphatic absorption of TG.

摘要

我们使用乳糜微粒形成抑制剂普朗尼克L-81(L-81),研究乳糜微粒形成是否参与膳食磷脂酰胆碱(PC)诱导的甘油三酯(TG)吸收增加。在大鼠中,将插管植入十二指肠(实验1和2)和肠系膜淋巴管(实验1),以3 ml/h的速率通过十二指肠插管输注含或不含L-81的乳化脂质溶液(大豆油,SO或大豆油加磷脂酰胆碱,LE),持续2小时,随后输注葡萄糖 - 氯化钠溶液2小时。收集肠系膜淋巴4小时(实验1)。在实验2中,在十二指肠输注测试脂质开始后20、40或90分钟收集小肠黏膜和内容物,以评估未插淋巴导管的大鼠黏膜中脂质的积累情况。在实验1中,在不使用L-81的情况下,两种测试脂质输注后淋巴TG输出迅速增加,但L-81消除了这些增加。在L-81处理下,TG在小肠黏膜中呈时间依赖性积累,但SO组和LE组的积累水平相似(实验2)。L-81处理的SO组和LE组之间小肠腔中剩余脂质的量没有差异。这些结果表明,LE不会增加脂质向黏膜细胞的摄取。我们得出结论,乳糜微粒的形成是膳食中高水平PC对TG淋巴吸收促进作用增加的原因。

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