Riisom T, Johnson S, Hill E G, Holman R T
J Lab Clin Med. 1981 Nov;98(5):764-75.
An evaluation of the EFAD syndrome in rats rendered diabetic with either alloxan or streptozotocin was performed. Diabetic rats fed an EFA-deficient diet for 7 or 13 weeks were less severely EFA-deficient than were nondiabetic rats fed EFA-deficient diet, as judged by dermal symptoms or by biochemical parameters such as the ratio of 20:3 omega 9/20:4 omega 6 (T/T ratio) and total fatty acids derived from linoleic acid. The T/T ratios of liver PL of diabetic EFA-deficient rats were lower than those of deficient control rats, and the ratios varied inversely with the blood glucose concentrations. The product/precursor ratios, arachidonic acid/linoleic acid, in liver PL were higher in diabetic deficient rats than in deficient control rats. Analysis of liver and heart PLs revealed higher arachidonic acid levels in the diabetic deficient rats than in the EFA-deficient controls, perhaps because of different growth rates. The activities of the delta 5, delta 6, and delta 9 desaturases were evaluated in liver microsomal systems. The delta 9 desaturase was depressed in diabetic rats in agreement with literature reports. The delta 6 desaturase, however, was slightly increased. The relative levels of delta 5, delta 6 and delta 9 desaturation products in liver and heart PLs did not parallel the measured desaturase activities of liver microsomes.
对用四氧嘧啶或链脲佐菌素诱导糖尿病的大鼠的必需脂肪酸缺乏综合征(EFAD)进行了评估。通过皮肤症状或生化参数(如20:3 ω9/20:4 ω6比例(T/T比例)和源自亚油酸的总脂肪酸)判断,喂食必需脂肪酸缺乏饮食7周或13周的糖尿病大鼠的必需脂肪酸缺乏程度不如喂食必需脂肪酸缺乏饮食的非糖尿病大鼠严重。糖尿病必需脂肪酸缺乏大鼠肝脏磷脂的T/T比例低于缺乏对照组大鼠,且该比例与血糖浓度呈反比。糖尿病缺乏大鼠肝脏磷脂中的花生四烯酸/亚油酸的产物/前体比例高于缺乏对照组大鼠。肝脏和心脏磷脂分析显示,糖尿病缺乏大鼠的花生四烯酸水平高于必需脂肪酸缺乏对照组,这可能是由于生长速率不同。在肝脏微粒体系统中评估了δ5、δ6和δ9去饱和酶的活性。与文献报道一致,糖尿病大鼠的δ9去饱和酶活性降低。然而,δ6去饱和酶活性略有增加。肝脏和心脏磷脂中δ5、δ6和δ9去饱和产物的相对水平与所测得的肝脏微粒体去饱和酶活性并不平行。