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首页> 外文期刊>American Journal of Physiology >High basal cell surface levels of fish GLUT4 are related to reduced sensitivity of insulin-induced translocation toward GGA and AS160 inhibition in adipocytes.
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High basal cell surface levels of fish GLUT4 are related to reduced sensitivity of insulin-induced translocation toward GGA and AS160 inhibition in adipocytes.

机译：鱼GLUT4的高基底细胞表面水平与胰岛素诱导的对GGA的易位敏感性降低以及脂肪细胞对AS160的抑制作用有关。

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摘要

Glucose entry into cells is mediated by a family of facilitative transporter proteins (GLUTs). In mammals, GLUT4 is expressed in insulin-sensitive tissues and is responsible for the postprandial uptake of glucose. In fish, GLUT4 also mediates insulin-regulated glucose entry into cells but differs from mammalian GLUT4 in its affinity for glucose and in protein motifs known to be important for the traffic of GLUT4. In this study, we have characterized the intracellular and plasma membrane (PM) traffic of two orthologs of GLUT4 in fish, trout (btGLUT4) and salmon (okGLUT4), that do not share the amino terminal FQQI targeting motif of mammalian GLUT4. btGLUT4 (FQHL) and, to a lesser extent, okGLUT4 (FQQL) showed higher basal PM levels, faster traffic to the PM after biosynthesis, and earlier acquisition of insulin responsiveness than rat GLUT4. Furthermore, btGLUT4 showed a similar profile of internalization than rat GLUT4. Expression of the dominant-interfering AS160-4P mutant caused a significant decrease in the insulin-induced PM levels of okGLUT4 and rat GLUT4 and, to a lesser extent, of btGLUT4, suggesting that btGLUT4 has reduced retention into the IRC. Contrary to rat GLUT4 and okGLUT4, the presence of btGLUT4 at the PM under insulin-stimulated conditions was not affected by coexpression of a dominant-interfering GGA mutant. These data suggest that fish GLUT4 follow a different trafficking pathway to the PM compared with rat GLUT4 that seems to be relatively independent of GGA. These results indicate that the regulated trafficking characteristics of GLUT4 have been modified during evolution from fish to mammals.
机译：葡萄糖进入细胞是由一类促进转运蛋白（GLUTs）介导的。在哺乳动物中，GLUT4在胰岛素敏感性组织中表达，并导致餐后葡萄糖摄取。在鱼类中，GLUT4还介导胰岛素调节的葡萄糖进入细胞，但与哺乳动物GLUT4的葡萄糖亲和力和已知对GLUT4的运输很重要的蛋白质基序不同。在这项研究中，我们已经表征了鱼类，鳟鱼（btGLUT4）和鲑鱼（okGLUT4）中两个GLUT4直系同源物的细胞内和质膜（PM）流量，它们不具有哺乳动物GLUT4的氨基末端FQQI靶向基序。与大鼠GLUT4相比，btGLUT4（FQHL）和较小的okGLUT4（FQQL）显示出更高的基础PM水平，生物合成后到达PM的流量更快，以及较早获得胰岛素反应性。此外，btGLUT4显示出与大鼠GLUT4类似的内化作用。显性干扰AS160-4P突变体的表达导致okGLUT4和大鼠GLUT4胰岛素诱导的PM水平显着降低，而btGLUT4的表达程度较小，这表明btGLUT4减少了对IRC的保留。与大鼠GLUT4和okGLUT4相反，在胰岛素刺激的条件下PM处btGLUT4的存在不受显性干扰GGA突变体共表达的影响。这些数据表明，与大鼠GLUT4似乎相对独立于GGA的鱼类相比，鱼GLUT4遵循不同的向PM的运输途径。这些结果表明，从鱼到哺乳动物的进化过程中，GLUT4的调节运输特性已被修饰。

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