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Diabetes increases facilitative glucose uptake and GLUT2 expression at the rat proximal tubule brush border membrane

机译:糖尿病会增加大鼠近端小管刷缘膜的葡萄糖摄取和GLUT2表达

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摘要

The mechanism of renal glucose transport involves the reabsorption of filtered glucose from the proximal tubule lumen across the brush border membrane (BBM) via a sodium-dependent transporter, SGLT, and exit across the basolateral membrane via facilitative, GLUT-mediated, transport. The aim of the present study was to determine the effect of streptozotocin-induced diabetes on BBM glucose transport. We found that diabetes increased facilitative glucose transport at the BBM by 67.5 % (P < 0.05) – an effect that was abolished by overnight fasting. Western blotting and immunohistochemistry demonstrated GLUT2 expression at the BBM during diabetes, but the protein was undetectable at the BBM of control animals or diabetic animals that had been fasted overnight. Our findings indicate that streptozotocin-induced diabetes causes the insertion of GLUT2 into the BBM and this may provide a low affinity/high capacity route of entry into proximal tubule cells during hyperglycaemia.
机译:肾脏葡萄糖转运的机制涉及通过钠依赖性转运蛋白SGLT从近端小管腔穿过刷状缘膜(BBM)重新吸收过滤后的葡萄糖,并通过促进性GLUT介导的转运穿过基底外侧膜。本研究的目的是确定链脲佐菌素诱导的糖尿病对BBM葡萄糖转运的影响。我们发现糖尿病使BBM的便利性葡萄糖转运增加了67.5%(P <0.05)-过夜禁食可消除这种影响。 Western印迹和免疫组织化学显示糖尿病期间BBM处有GLUT2表达,但禁食过夜的对照动物或糖尿病动物的BBM处未检测到该蛋白。我们的发现表明,链脲佐菌素诱导的糖尿病会导致GLUT2插入BBM中,这可能在高血糖症期间提供低亲和力/高容量进入近端小管细胞的途径。

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