Transmissible Gastroenteritis Virus Infection Enhances SGLT1 and GLUT2 Expression to Increase Glucose Uptake.
Transmissible Gastroenteritis Virus Infection Enhances SGLT1 and GLUT2 Expression to Increase Glucose Uptake.
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DOI：
10.1371/journal.pone.0165585
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Yang Q
中科院分区：
文献类型：
--
作者：
Dai L;Hu WW;Xia L;Xia M;Yang Q
传染性胃肠炎病毒（TGEV）是一种冠状病毒，可导致绒毛萎缩，随后是隐窝增生，降低肠道消化酶的活性，并破坏肠道营养物质的吸收。在体内，TGEV主要靶向并感染肠上皮细胞，肠上皮细胞分别通过顶端和基底侧转运蛋白Na+依赖性葡萄糖转运蛋白1（SGLT 1）和促进性葡萄糖转运蛋白2（GLUT 2）在葡萄糖吸收中发挥重要作用。因此，在这项研究中，我们试图评估TGEV感染对葡萄糖摄取和SGLT 1和GLUT 2表达的影响。我们的数据表明，TGEV感染导致葡萄糖摄取增加，EGFR、SGLT 1和GLUT 2表达增强。此外，抑制研究表明，EGFR调节葡萄糖摄取在控制和TGEV感染的细胞。最后，随后发现高葡萄糖吸收促进TGEV复制。
Transmissible gastroenteritis virus (TGEV) is a coronavirus that causes villus atrophy, followed by crypt hyperplasia, reduces the activities of intestinal digestive enzymes, and disrupts the absorption of intestinal nutrients. In vivo, TGEV primarily targets and infects intestinal epithelial cells, which play an important role in glucose absorption via the apical and basolateral transporters Na+-dependent glucose transporter 1 (SGLT1) and facilitative glucose transporter 2 (GLUT2), respectively. In this study, we therefore sought to evaluate the effects of TGEV infection on glucose uptake and SGLT1 and GLUT2 expression. Our data demonstrate that infection with TGEV resulted in increased glucose uptake and augmented expression of EGFR, SGLT1 and GLUT2. Moreover, inhibition studies showed that EGFR modulated glucose uptake in control and TGEV infected cells. Finally, high glucose absorption was subsequently found to promote TGEV replication.