Blank M E, Bode F, Huland E, Diedrich D F, Baumann K
Biochim Biophys Acta. 1985 Mar 21;844(3):314-9. doi: 10.1016/0167-4889(85)90132-6.
Renal brush-border membrane vesicles prepared from streptozotocin-induced 4-day-diabetic rats possessed a Na+-dependent D-glucose transport system that exhibited apparent Kt and Vmax values about 2-fold greater than normal. Apparently, hyperglycemia and probably other stimuli cause the induction and membrane incorporation of a low-affinity transporter in these membranes; this increased sugar-transport capacity is retained for at least 4 weeks so long as the animals maintained or increased their body weight. Membranes prepared from 28-day-diabetic, severely ill ketoacidotic animals lose this enhanced transport ability and the decrease in Vmax was found to correlate directly with the weight loss. Furthermore, the transporter in brush-border membranes prepared from these cachectic animals had an even lower affinity for glucose than those from the acute hyperglycemic animals. That these changes in the diabetic animals represent major alterations in renal brush-border membrane construction is further supported by our observation that the specific activity of the marker enzymes, alkaline phosphatase and neutral alpha-glucosidase, are profoundly increased and decreased, respectively, in this condition.
从链脲佐菌素诱导的糖尿病4天大鼠制备的肾刷状缘膜囊泡具有一种依赖于Na⁺的D-葡萄糖转运系统,其表观米氏常数(Kt)和最大转运速率(Vmax)值比正常情况大约高2倍。显然,高血糖以及可能的其他刺激导致这些膜中低亲和力转运体的诱导和膜整合;只要动物维持或增加体重,这种增加的糖转运能力至少可保留4周。从28天糖尿病、严重酮症酸中毒的患病动物制备的膜失去了这种增强的转运能力,并且发现Vmax的降低与体重减轻直接相关。此外,从这些恶病质动物制备的刷状缘膜中的转运体对葡萄糖的亲和力甚至低于急性高血糖动物的转运体。我们观察到在这种情况下,标记酶碱性磷酸酶和中性α-葡萄糖苷酶的比活性分别显著增加和降低,这进一步支持了糖尿病动物中的这些变化代表肾刷状缘膜结构的主要改变这一观点。