Nelson G J, Kelley D S, Emken E A, Phinney S D, Kyle D, Ferretti A
Western Human Nutrition Research Center, ARS, USDA, San Francisco, California 94129, USA.
Lipids. 1997 Apr;32(4):415-20. doi: 10.1007/s11745-997-0054-8.
While there are many reports of studies that fed arachidonic acid (AA) to animals, there are very few reports of AA feeding to humans under controlled conditions. This 130-d study was conceived as a controlled, symmetrical crossover design with healthy, adult male volunteers. They lived in the metabolic research unit (MRU) of the Western Human Nutrition Research (WHNRC) for the entire study. All food was prepared by the WHNRC kitchen. The basal (low-AA) diet consisted of natural foods (30 en% fat, 15 en% protein, and 55 en% carbohydrate), containing 210 mg/d of AA, and met the recommended daily allowance for all nutrients. The high-AA (intervention) diet was similar except that 1.5 g/d of AA in the form of a triglyceride containing 50% AA replaced an equal amount of high-oleic safflower oil in the basal diet. The subjects (ages 20 to 39) were within -10 to +20% of ideal body weight, nonsmoking, and not allowed alcohol in the MRU. Their exercise level was constant, and their body weights were maintained within 2% of entry level. Subjects were initially fed the low-AA diet for 15 d. On day 16, half of the subjects (group A) wee placed on the high-AA diet, and the other group (B) remained on the low-AA diets. On day 65, the two groups switched diets. On day 115, group B returned to the low-AA diet. This design, assuming no carryover effect, allowed us to merge the data from the two groups, with the data comparison days being 65 (low-AA) and 115 (high-AA) for group B and 130 (low-AA) and 65 (high-AA) for group A. The main indices studied were the fatty acid composition of the plasma, red blood cells, platelets, and adipose tissue; in vitro platelet aggregation, bleeding times, clotting factors; immune response as measured by delayed hypersensitivity skin tests, cellular proliferation of peripheral blood mononuclear cells in response to various mitogens and antigens, natural killer cell activity, and response to measles/mumps/rubella and influenza vaccines; the metabolic conversion of deuterated linoleic acid to AA and the metabolic fate of deuterated AA in the subjects on and off the high-AA diet; and the production of eicosanoids as measured by excretion of 11-DTXB2 and PGI2-M in urine. The results of these studies will be presented in the next five papers from this symposium.
虽然有许多关于给动物喂食花生四烯酸（AA）的研究报告，但在可控条件下给人类喂食AA的报告却非常少。这项为期130天的研究采用了针对健康成年男性志愿者的可控对称交叉设计。在整个研究过程中，他们居住在西部人类营养研究中心（WHNRC）的代谢研究单元（MRU）。所有食物均由WHNRC厨房制备。基础（低AA）饮食由天然食物组成（30能量%脂肪、15能量%蛋白质和55能量%碳水化合物），含有210毫克/天的AA，并且满足所有营养素的推荐每日摄入量。高AA（干预）饮食与之相似，只是在基础饮食中，以含有50%AA的甘油三酯形式存在的1.5克/天的AA替代了等量的高油酸红花油。受试者（年龄在20至39岁之间）的体重在理想体重的-10%至+20%范围内，不吸烟，且在MRU内不允许饮酒。他们的运动水平保持恒定，体重维持在初始水平的2%以内。受试者最初食用低AA饮食15天。在第16天，一半的受试者（A组）开始食用高AA饮食，另一组（B组）继续食用低AA饮食。在第65天，两组交换饮食。在第115天，B组恢复食用低AA饮食。这种设计在假设没有残留效应的情况下，使我们能够合并两组的数据，对于B组，数据比较日为第65天（低AA）和第115天（高AA），对于A组，数据比较日为第130天（低AA）和第65天（高AA）。所研究的主要指标包括血浆、红细胞、血小板和脂肪组织的脂肪酸组成；体外血小板聚集、出血时间、凝血因子；通过迟发型超敏皮肤试验、外周血单个核细胞对各种有丝分裂原和抗原的细胞增殖、自然杀伤细胞活性以及对麻疹/腮腺炎/风疹和流感疫苗的反应来衡量的免疫反应；在食用和停用高AA饮食的受试者中，氘代亚油酸向AA的代谢转化以及氘代AA的代谢命运；以及通过尿液中11-DTXB2和PGI2-M的排泄来衡量的类花生酸的产生。这些研究的结果将在本次研讨会接下来的五篇论文中呈现。
