Satchithanandam S, Flynn T J, Calvert R J, Kritchevsky D
Division of Science and Applied Technology, US Food and Drug Administration, Laurel, Maryland 20708, USA.
Lipids. 1999 Dec;34(12):1305-11. doi: 10.1007/s11745-999-0482-5.
Peanut oil was shown to be atherogenic in cholesterol-fed rats, rabbits, and monkeys. However, after randomization, a process in which the fatty acids in peanut oil are randomly rearranged, its atherogenicity was significantly reduced in cholesterol-fed rabbits and monkeys. The mechanism for this effect remains unknown. This study was designed to investigate whether the absorption, transport and distribution of dietary cholesterol and oleic acid in the lymph were altered in the presence of peanut oil or randomized peanut oil. Previous investigators collected lymph through the mesenteric duct for 6 h and analyzed lymph for cholesterol. In the present study, lymph fluids were collected at timed intervals for up to 8 h and then at 24 h via the thoracic duct. Cholesterol and oleic acid (fatty acid) were estimated not only in the whole lymph but also in lymph lipoprotein fractions and in major lipid fractions. A 24-h lymph collection will enhance accuracy as short-term fluctuations in lipid absorption will not affect the results. Thoracic duct lymph collection is quantitative compared to mesenteric duct lymph collection, which provides only a fraction of the total lymph. Rats were given a lipid emulsion containing either peanut oil or randomized peanut oil. The emulsion also contained cholesterol, oleic acid, and sodium taurocholate in saline and was given through a duodenal catheter. Results show that absorption, transport, and distribution of cholesterol and oleic acid in the lymph fluids were similar in both dietary groups. These results suggest that the atherogenicity of peanut oil may be due to other events taking place subsequent to the release of cholesterol-containing chylomicrons and very low density lipoprotein by the small intestinal epithelial cells into the blood or may be due to the triglyceride structure itself.
花生油在喂食胆固醇的大鼠、兔子和猴子中显示出致动脉粥样硬化作用。然而,经过随机化处理(在该过程中花生油中的脂肪酸会随机重新排列)后,其在喂食胆固醇的兔子和猴子中的致动脉粥样硬化性显著降低。这种作用的机制尚不清楚。本研究旨在调查在存在花生油或随机化花生油的情况下,膳食胆固醇和油酸在淋巴中的吸收、运输和分布是否发生改变。先前的研究人员通过肠系膜导管收集淋巴6小时,并分析淋巴中的胆固醇。在本研究中,每隔一定时间收集淋巴液长达8小时,然后在24小时时通过胸导管收集。不仅在全淋巴中,而且在淋巴脂蛋白组分和主要脂质组分中估计胆固醇和油酸(脂肪酸)。24小时的淋巴收集将提高准确性,因为脂质吸收的短期波动不会影响结果。与仅提供总淋巴一部分的肠系膜导管淋巴收集相比,胸导管淋巴收集是定量的。给大鼠喂食含有花生油或随机化花生油的脂质乳剂。该乳剂还在盐水中含有胆固醇、油酸和牛磺胆酸钠,并通过十二指肠导管给予。结果表明,两个饮食组淋巴液中胆固醇和油酸的吸收、运输和分布相似。这些结果表明,花生油的致动脉粥样硬化性可能是由于小肠上皮细胞将含胆固醇的乳糜微粒和极低密度脂蛋白释放到血液后发生的其他事件,或者可能是由于甘油三酯结构本身。