Vidal J C, McIntyre J O, Churchill P, Andrew J A, Péhuet M, Fleischer S
Arch Biochem Biophys. 1983 Jul 15;224(2):643-58. doi: 10.1016/0003-9861(83)90252-7.
Liver mitochondria and submitochondrial vesicles have been prepared from rats made diabetic by treatment with streptozotocin (diabetic membranes). The membranes were characterized in terms of phospholipid and fatty acid composition, electron transport functions, and D-beta-hydroxybutyrate dehydrogenase activity and compared with mitochondria and submitochondrial vesicles prepared from control animals (control membranes). No change in the phospholipid composition (44% lecithin, 35% phosphatidylethanolamine, and 21% diphosphatidylglycerol) was found, but a marked alteration in fatty acid composition of both the total phospholipid and lecithin occurred within 3 weeks after streptozotozin treatment and persisted thereafter. In lecithin, the 18:1/18:0 ratio decreases approximately 33% and the 20:4/18:2 ratio decreases approximately 55%. D-beta-hydroxybutyrate dehydrogenase is a lipid-requiring enzyme which has a specific requirement of lecithin for function. In diabetic membranes, there is a progressive decrease in D-beta-hydroxybutyrate dehydrogenase activity with time after streptozotocin treatment to about 40% of control value at 15 weeks. In contrast, succinate oxidase and succinate- or NADH-cytochrome c reductase activities remain essentially unaltered. Further, the Arrhenius plot characteristics differ for D-beta-hydroxybutyrate dehydrogenase in diabetic membranes as compared with control membranes, in that the break point of the biphasic plot increases from 20 +/- 1 degree C in controls to 29 +/- 1 degree C in samples from diabetic animals. The change occurs about 3 weeks after streptozotocin treatment and is correlatable with the increased saturation of the fatty acid moiety of the phospholipids. The observed changes in D-beta-hydroxybutyrate dehydrogenase function and phospholipid composition were prevented by administration of insulin to the diabetic animals and are therefore referable to insulin insufficiency.
已从用链脲佐菌素治疗制成糖尿病的大鼠中制备了肝线粒体和亚线粒体小泡（糖尿病膜）。对这些膜的磷脂和脂肪酸组成、电子传递功能以及D-β-羟基丁酸脱氢酶活性进行了表征，并与从对照动物制备的线粒体和亚线粒体小泡（对照膜）进行了比较。未发现磷脂组成有变化（44%卵磷脂、35%磷脂酰乙醇胺和21%二磷脂酰甘油），但在链脲佐菌素治疗后3周内，总磷脂和卵磷脂的脂肪酸组成发生了显著改变，并持续存在。在卵磷脂中，18:1/18:0比例降低约33%，20:4/18:2比例降低约55%。D-β-羟基丁酸脱氢酶是一种需要脂质的酶，其功能对卵磷脂有特定需求。在糖尿病膜中，链脲佐菌素治疗后，D-β-羟基丁酸脱氢酶活性随时间逐渐降低，在15周时降至对照值的约40%。相比之下，琥珀酸氧化酶以及琥珀酸或NADH-细胞色素c还原酶活性基本保持不变。此外，与对照膜相比，糖尿病膜中D-β-羟基丁酸脱氢酶的阿伦尼乌斯图特征不同，即双相图的转折点从对照中的20±1℃增加到糖尿病动物样品中的29±1℃。这种变化发生在链脲佐菌素治疗后约3周，并且与磷脂脂肪酸部分饱和度的增加相关。给糖尿病动物注射胰岛素可防止观察到的D-β-羟基丁酸脱氢酶功能和磷脂组成的变化，因此这些变化归因于胰岛素不足。
