Ziboh V A, Hsia S L
J Lipid Res. 1972 Jul;13(4):458-67.
Severe scaly lesions in the skin, especially in the feet and tail, of the rat were induced by feeding a diet deficient in essential fatty acids (EFA). Analysis of the fatty acids in skin lipids of these EFA-deficient rats showed a marked increase of monoenoic acids (16:1 and 18:1) and eicosatrienoic acid (20:3), with concomitant decreases of dienoic acid (18:2) and tetraenoic acid (20:4). Topical application of prostaglandin E(2) (PGE(2)) to the scaly lesions resulted in clearance of the lesions, but did not significantly alter the composition of fatty acids in the skin. Intraperitoneal injection of PGE(2) had no observable effect on the skin lesions. Furthermore, incubation of skin specimens from the EFA-deficient rats with (14)C-labeled glucose showed a 4-5-fold increase of incorporation of glucose carbon into lipid fractions, particularly the sterol esters, and a 3-4-fold increase in pentose cycle activity. Addition of PGE(2) to the incubation mixture resulted in approximately 70% inhibition of sterol ester biosynthesis by skin of the EFA-deficient rats. These results suggest that the effects of PGE(2) in clearing the scales may be associated with its inhibitory effect on abnormal sterol esterification in the skin of the EFA-deficient rats.
通过给大鼠喂食缺乏必需脂肪酸(EFA)的饲料,可诱发其皮肤出现严重的鳞屑性病变,尤其是足部和尾部。对这些EFA缺乏大鼠皮肤脂质中的脂肪酸分析显示,单烯酸(16:1和18:1)和二十碳三烯酸(20:3)显著增加,同时二烯酸(18:2)和四烯酸(20:4)减少。将前列腺素E2(PGE2)局部应用于鳞屑性病变可使病变消退,但并未显著改变皮肤中脂肪酸的组成。腹腔注射PGE2对皮肤病变无明显影响。此外,用(14)C标记的葡萄糖孵育EFA缺乏大鼠的皮肤标本,结果显示葡萄糖碳掺入脂质组分,尤其是甾醇酯的量增加了4 - 5倍,戊糖循环活性增加了3 - 4倍。向孵育混合物中添加PGE2可使EFA缺乏大鼠皮肤的甾醇酯生物合成受到约70%的抑制。这些结果表明,PGE2清除鳞屑的作用可能与其对EFA缺乏大鼠皮肤中异常甾醇酯化的抑制作用有关。