Mann N J, Warrick G E, O'Dea K, Knapp H R, Sinclair A J
School of Nutrition and Public Health, Deakin University, Geelong, Victoria, Australia.
Lipids. 1994 Mar;29(3):157-62. doi: 10.1007/BF02536723.
We examined the effect of dietary supplementation of linoleic acid (LA), arachidonic acid (AA) or eicosapentaenoic acid (EPA) to rats fed a diet low in linoleic acid on in vitro and in vivo production of prostacyclin. Male Sprague Dawley rats were fed a high-fat diet (50% energy as fat, 1.5% linoleic acid) for two weeks. Three of the groups were then supplemented orally with either 90 mg/d of LA, AA or EPA, all as the ethyl esters, for a further two weeks while remaining on the high-fat diet. Forty-eight hour urine samples were collected at the end of the second and fourth weeks. In vivo prostacyclin production was determined by a stable isotope dilution, gas chromatography/mass spectrometry assay for the major urinary metabolite of prostacyclins (2,3-dinor-6-keto-PGF1 alpha or PGI2-M and delta 17-2,3-dinor-6-keto-PGF1 alpha or PGI3-M). In vitro prostacyclin production was determined by radioimmunoassay of the stable metabolite (6-keto-PGF 1 alpha) following incubation of arterial tissue. Oral supplementation with AA resulted in a rise in plasma and aorta 20:4n-6, and increased in vitro prostacyclin and urinary PGI2-M production. EPA supplementation resulted in a rise in plasma and aorta 20:5n-3 and 22:5n-3, and a decline in plasma 20:4n-6, but not in the aorta. In the EPA-supplemented group, the in vitro prostacyclin and the urinary PGI3-M increased, but urinary PGI2-M decreased. The increase in in vitro prostacyclin production in the EPA-supplemented rats was unexpected and without obvious explanation.(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了在喂食低亚油酸饮食的大鼠中,膳食补充亚油酸(LA)、花生四烯酸(AA)或二十碳五烯酸(EPA)对前列环素体外和体内生成的影响。雄性斯普拉格-道利大鼠喂食高脂饮食(50%的能量来自脂肪,1.5%亚油酸)两周。然后,其中三组大鼠继续食用高脂饮食,同时口服补充90毫克/天的LA、AA或EPA(均为乙酯形式),持续两周。在第二周和第四周结束时收集48小时尿液样本。通过稳定同位素稀释、气相色谱/质谱分析法测定前列环素主要尿代谢产物(2,3-二去甲-6-酮-前列腺素F1α或PGI2-M以及δ17-2,3-二去甲-6-酮-前列腺素F1α或PGI3-M)来确定体内前列环素的生成。通过对动脉组织孵育后的稳定代谢产物(6-酮-前列腺素F1α)进行放射免疫测定来确定体外前列环素的生成。口服补充AA导致血浆和主动脉中20:4n-6升高,并增加体外前列环素和尿中PGI2-M的生成。补充EPA导致血浆和主动脉中20:5n-3和22:5n-3升高,血浆中20:4n-6下降,但主动脉中未下降。在补充EPA的组中,体外前列环素和尿中PGI3-M增加,但尿中PGI2-M减少。补充EPA的大鼠体外前列环素生成增加出乎意料且无明显解释。(摘要截短至250字)