Chinn K S, Welsch D J, Salsgiver W J, Mehta A, Raz A, Obukowicz M G
G.D. Searle, St. Louis, Missouri 63198, USA.
Lipids. 1997 Sep;32(9):979-88. doi: 10.1007/s11745-997-0128-7.
Controlled feeding of linoleic acid (LA) or arachidonic acid (AA) to essential fatty acid-deficient (EFAD) rats was used to define the relationship between dietary AA and the inflammatory response evoked during adjuvant-induced arthritis. Based on energy percentage, EFAD rats were fed AA at the human daily equivalent (1x; 5.5 mg/day) or 10 times that amount (10x; 55 mg/day) or, alternatively 0.5x of LA (273 mg/day). Feeding of 0.5x LA restored the plasma level of AA to that in chow-fed controls. In contrast, feeding of 1x AA only partially restored the plasma level of AA; 10x AA was required to fully replete AA. In parallel to the degree of repletion of AA in plasma, there were accompanying decreases in the levels of palmitoleic acid, oleic acid, and Mead acid. Compared to rats fed the standard laboratory chow diet (Control), edema in the primary hind footpads was decreased by 87% in EFAD, 71% in EFAD + 1x AA, 45% in EFAD + 10x AA, and 30% in EFAD + 0.5x LA. The decrease in edema in the footpads of EFAD rats was nearly identical to the decrease in edema in the footpads of Control rats dosed with indomethacin. Hind footpad edema correlated with the final AA plasma level and eicosanoid levels extracted from hind footpad tissue, but not with neutrophil infiltration. The data showed that 0.5x LA and 10x AA, but not 1x AA, could quickly replete AA, accompanied by the synthesis of AA-derived eicosanoids and restoration of edema. These results suggest that in humans consumption of the average daily amount of AA without concurrent ingestion of LA would not alleviate an EFAD state.
通过对必需脂肪酸缺乏（EFAD）大鼠进行亚油酸（LA）或花生四烯酸（AA）的对照喂养，来确定膳食中AA与佐剂诱导性关节炎期间诱发的炎症反应之间的关系。基于能量百分比，给EFAD大鼠喂食人类每日等量的AA（1倍；5.5毫克/天）或该量的10倍（10倍；55毫克/天），或者替代地喂食0.5倍的LA（273毫克/天）。喂食0.5倍LA可使AA的血浆水平恢复到正常饮食对照组的水平。相比之下，喂食1倍AA仅部分恢复了AA的血浆水平；需要10倍AA才能使AA完全充足。与血浆中AA的充足程度平行，棕榈油酸、油酸和玛德酸的水平也随之降低。与喂食标准实验室普通饮食的大鼠（对照）相比，EFAD大鼠后足垫的水肿减少了87%，EFAD + 1倍AA组减少了71%，EFAD + 10倍AA组减少了45%，EFAD + 0.5倍LA组减少了30%。EFAD大鼠足垫水肿的减少与用吲哚美辛给药的对照大鼠足垫水肿的减少几乎相同。后足垫水肿与最终的AA血浆水平以及从后足垫组织中提取的类二十烷酸水平相关，但与中性粒细胞浸润无关。数据表明，0.5倍LA和10倍AA，但不是1倍AA，可以快速补充AA，同时伴随着AA衍生的类二十烷酸的合成和水肿的恢复。这些结果表明，在人类中，不同时摄入LA而仅食用平均每日量的AA并不能缓解必需脂肪酸缺乏状态。
