Prasad M R, Joshi V C
J Biol Chem. 1979 Feb 25;254(4):997-9.
The rat hepatic stearoyl-CoA desaturation decreased by 3.7-fold in streptozotocin-induced diabetes. Insulin treatment of diabetic rats increased the enzyme activity by 7-fold. In marked contrast to glucose administration, fructose feeding in diabetic rats resulted in 20-fold stimulation of stearoyl-CoA desaturation, although both carbohydrates stimulated stearoyl-CoA desaturation in normal rats. Measurement of the microsomal electron transfer components showed no significant changes in the NADH-cytochrome b5 reductase activity or in the concentration of cytochrome b5. However, the activity of the terminal desaturase changed in a parallel fashion as the amount of terminal desaturase reflect changes in the overall desaturation. Supplementation of various microsomes with the saturating amount of purified terminal desaturase resulted in the formation of similar amounts of catalytically active complex and increased the stearoyl-CoA desaturation to the same level suggesting that the changes in the amount of terminal desaturase reflect changes in the overall desaturation. The results support the suggestion that both insulin and the intermediates of carbohydrate metabolism are involved in the regulation of terminal desaturase.
在链脲佐菌素诱导的糖尿病大鼠中,肝脏硬脂酰辅酶A去饱和酶活性降低了3.7倍。对糖尿病大鼠进行胰岛素治疗可使该酶活性增加7倍。与给予葡萄糖形成显著对比的是,给糖尿病大鼠喂食果糖可使硬脂酰辅酶A去饱和酶活性提高20倍,尽管这两种碳水化合物在正常大鼠中均能刺激硬脂酰辅酶A去饱和酶活性。微粒体电子传递成分的测定显示,NADH - 细胞色素b5还原酶活性或细胞色素b5浓度均无显著变化。然而,末端去饱和酶的活性变化与末端去饱和酶的量呈平行关系,因为末端去饱和酶的量反映了总体去饱和的变化。用饱和量的纯化末端去饱和酶补充各种微粒体,会形成相似量的具有催化活性的复合物,并使硬脂酰辅酶A去饱和酶活性提高到相同水平,这表明末端去饱和酶量的变化反映了总体去饱和的变化。这些结果支持了胰岛素和碳水化合物代谢中间产物均参与末端去饱和酶调节的观点。