Studies on the regulation of fatty acid biosynthesis by drugs

研究了纤维酸和脱氢表雄酮（DHEA）对油酸形成的影响，并与糖尿病或碳水化合物联合使用。纤维酸和脱氢表雄酮均引起油酸增加，亚油酸和二十二碳六烯酸减少。碳水化合物处理后，油酸和棕榈油酸的比例增加，亚油酸和花生四烯酸的比例降低。脱氢表雄酮、碳水化合物和纤维酸均能提高△9去饱和酶（SCD）和棕榈酰辅酶a链延长酶（PCE）的活性。纤维素酸与碳水化合物复合处理对两种酶的诱导作用不同。在相同条件下，油酸的比例有所提高。在糖尿病状态下，SCD和PCE均有活性，而葡萄糖无。尽管脱氢表雄酮在体外诱导线粒体和过氧化物酶体中负责脂肪酸氧化的酶，但脱氢表雄酮加速了线粒体中的脂肪酸氧化。上述结果表明，SCD和PCE是由不同条件诱导的，但不同条件下脂肪酸组成不同。不同的脂肪酸诱导量和消耗量可能会对脂肪酸组成产生不同的影响。

Effects of clofibric acid and dehydroepiandrosterone (DHEA) on the formation of oleic acid was studied in combination with diabetes or carbohydrate administration. Both clofibric acid and DHEA caused an increase in oleic acid and a decrease in linoleic acid and docosahexaenoic acid. By contrast, the proportion of oleic acid and palmitoleic acid was increased while the proportion of linoleic acid and arachidonic acid decreased upon carbohydrate administration. The activities of △9 desaturase (SCD) and palmitoyl-CoA chain elongase (PCE) were increased by DHEA, carbohydrate and clofibric acid. The induction of both enzymes were different when clofibric acid was treated in combination with carbohydrate. The proportion of oleic acid was increased at the same condition. In diabetic state, both SCD and PCE activities while glucose did not. DHEA accelerated fatty acid oxidation in mitochondria despite that DHEA induced the enzymes responsible for fatty acid oxidation in both mitochondria and peroxisomes in vitro.The above results suggest that SCD and PCE were induced by various conditions, however, fatty acid composition differed between the conditions. Different induction and consumption of fatty acid may be responsible for different effects on fatty acid composition.