Kurokawa T, Hashida F, Kawabata S, Ishibashi S
Department of Physiological Chemistry, Hiroshima University School of Medicine, Japan.
Biochem Mol Biol Int. 1995 Sep;37(1):33-8.
The small intestinal sodium dependent absorption of D-glucose has been known to be increased by diabetes mellitus. Furthermore, we previously showed that the enhanced activity of Na+/glucose cotransporter (SGLT1) was restored by the treatment with insulin. The present study was designed to investigate the mechanism by which diabetes mellitus and insulin regulated the activity of the small intestinal SGLT1. The acute diabetes at 2 weeks after the injection of streptozotocin increased the expression of SGLT1 protein in rat small intestinal brush border membrane vesicles without changing the mRNA level for SGLT1. In addition, we showed that the increased content of SGLT1 protein was restored by the subcutaneous treatment with insulin. In contrast, there was no change of the mRNA level for SGLT1 in diabetic and insulin-treated diabetic rats. These results suggest that rat intestinal SGLT1 activity is under the translational or posttranslational controls by insulin.
已知糖尿病会增加小肠对D-葡萄糖的钠依赖性吸收。此外,我们之前表明,用胰岛素治疗可恢复钠/葡萄糖协同转运蛋白(SGLT1)增强的活性。本研究旨在探讨糖尿病和胰岛素调节小肠SGLT1活性的机制。注射链脲佐菌素2周后的急性糖尿病增加了大鼠小肠刷状缘膜囊泡中SGLT1蛋白的表达,而SGLT1的mRNA水平没有变化。此外,我们表明皮下注射胰岛素可恢复SGLT1蛋白增加的含量。相比之下,糖尿病大鼠和胰岛素治疗的糖尿病大鼠中SGLT1的mRNA水平没有变化。这些结果表明,大鼠肠道SGLT1活性受胰岛素的翻译或翻译后调控。