Rogers K S, Higgins E S, Kline E S
Biochem Med Metab Biol. 1986 Aug;36(1):91-7. doi: 10.1016/0885-4505(86)90111-8.
The streptozotocin diabetic rat was selected as a model to study how insulin deficiency alters vitamin B6 utilization by focusing on pyridoxal phosphate levels and aspartate aminotransferase activities in liver tissues. Diabetes of 15 weeks' duration lowered plasma pyridoxal phosphate levels by 84%. Normal plasma pyridoxal phosphate was 480 pmole/ml. Fractionation of liver into mitochondrial and extramitochondrial compartments demonstrated that diabetes caused a 43% diminution in mitochondrial pyridoxal phosphate per gram of liver. There was no cytoplasmic change in these diabetic rats. Mitochondrial aspartate aminotransferase activity was decreased 53% per gram of diabetic liver and cytoplasmic aspartate aminotransferase activity was elevated 3.4-fold. Damage to diabetic mitochondria during preparation procedures could not account for the rise in cytoplasmic aspartate aminotransferase activity. Electrophoresis showed that in the diabetic cytoplasm both cathodal and anodal forms of the enzyme were elevated. Speculations concerning mitochondrial loss and cytoplasmic gain of enzyme activity as well as those on the reduction of plasma pyridoxal phosphate in the diabetic rat are presented.
选择链脲佐菌素诱导的糖尿病大鼠作为模型，通过关注肝组织中磷酸吡哆醛水平和天冬氨酸转氨酶活性，研究胰岛素缺乏如何改变维生素B6的利用。病程15周的糖尿病使血浆磷酸吡哆醛水平降低了84%。正常血浆磷酸吡哆醛水平为480皮摩尔/毫升。将肝脏分离为线粒体和线粒体外部分，结果显示糖尿病导致每克肝脏中线粒体磷酸吡哆醛减少43%。这些糖尿病大鼠的细胞质没有变化。每克糖尿病肝脏中线粒体天冬氨酸转氨酶活性降低53%，而细胞质天冬氨酸转氨酶活性升高3.4倍。制备过程中糖尿病线粒体的损伤无法解释细胞质天冬氨酸转氨酶活性的升高。电泳显示，在糖尿病细胞质中，该酶的阴极和阳极形式均升高。文中还对糖尿病大鼠线粒体酶活性丧失和细胞质酶活性增加以及血浆磷酸吡哆醛降低的情况进行了推测。
