Orellana M, Valdés E, Del Villar E
Department of Biochemistry, Faculty of Medicine, University of Chile, Santiago, Chile.
Gen Pharmacol. 1997 Mar;28(3):361-4. doi: 10.1016/s0306-3623(96)00231-5.
Microsomal lauric acid hydroxylation and fatty acid peroxisomal beta-oxidation were studied in hepatic subcellulant preparations from streptozotocin-induced diabetic and diabetic insulin-treated rats. 2. The liver microsomes of the streptozotocin diabetic rats displayed a similar activity to hydroxylate lauric acid as the control microsomes. 3. Diabetic insulin-treated rats showed lower (omega 1) and omega-lauric acid hydroxylase activities than diabetic and control rats. 4. Streptozotocin-induced diabetes and diabetic insulin-treated rats exhibited no significant changes on peroxisomal palmitoyl CoA beta-oxidation compared to the control rats. 5. Both microsomal and peroxisomal fatty acid oxidation responded in a similar way in this model of experimental diabetes.
在链脲佐菌素诱导的糖尿病大鼠和糖尿病胰岛素治疗大鼠的肝亚细胞制剂中,研究了微粒体月桂酸羟基化和脂肪酸过氧化物酶体β氧化。2. 链脲佐菌素糖尿病大鼠的肝微粒体显示出与对照微粒体相似的月桂酸羟基化活性。3. 糖尿病胰岛素治疗大鼠的ω1和ω-月桂酸羟化酶活性低于糖尿病大鼠和对照大鼠。4. 与对照大鼠相比,链脲佐菌素诱导的糖尿病大鼠和糖尿病胰岛素治疗大鼠的过氧化物酶体棕榈酰辅酶Aβ氧化无显著变化。5. 在该实验性糖尿病模型中,微粒体和过氧化物酶体脂肪酸氧化的反应方式相似。