GLUT8 is a glucose transporter responsible for insulin-stimulated glucose uptake in the blastocyst
GLUT8 is a glucose transporter responsible for insulin-stimulated glucose uptake in the blastocyst
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DOI：
10.1073/pnas.97.13.7313
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发表时间：
2000-06-20
影响因子：
11.1
通讯作者：
Moley, KH
中科院分区：
文献类型：
--
作者：
Carayannopoulos, MO;Chi, MMY;Moley, KH
哺乳动物植入前囊胚表现出胰岛素刺激的葡萄糖摄取，尽管缺乏唯一已知的胰岛素调节转运蛋白，GLUT 4，我们描述了一个以前未鉴定的成员的哺乳动物促进GLUT超家族，表现出约20-25%的同一性与其他小鼠促进GLUT。胰岛素诱导该蛋白质的细胞内定位的变化，其转化为囊胚中葡萄糖摄取的增加。这一过程被反义寡探针抑制。这种转运蛋白的存在对于成功的胚泡发育、燃料代谢和随后的着床可能是必要的。此外，替代转运蛋白的存在可以解释在其他组织中胰岛素调节的葡萄糖转运在GLUT 4的情况下的例子。
Mammalian preimplantation blastocysts exhibit insulin-stimulated glucose uptake despite the absence of the only known insulin-regulated transporter, GLUT4, We describe a previously unidentified member of the mammalian facilitative GLUT superfamily that exhibits approximate to 20-25% identity with other murine facilitative GLUTs. Insulin induces a change in the intracellular localization of this protein, which translates into increased glucose uptake into the blastocyst. a process that is inhibited by antisense oligoprobes. Presence of this transporter may be necessary for successful blastocyst development, fuel metabolism, and subsequent implantation. Moreover, the existence of an alternative transporter may explain examples in other tissues of insulin-regulated glucose transport in the absence of GLUT4.