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首页> 外文期刊>Cell metabolism >The cancer-associated FGFR4-G388R polymorphism enhances pancreatic insulin secretion and modifies the risk of diabetes
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The cancer-associated FGFR4-G388R polymorphism enhances pancreatic insulin secretion and modifies the risk of diabetes

机译：癌症相关的FGFR4-G388R多态性增强了胰腺胰岛素的分泌并改变了患糖尿病的风险

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The fibroblast growth factor receptor 4 (FGFR4)-R388 single-nucleotide polymorphism has been associated with cancer risk and prognosis. Here we show that the FGFR4-R388 allele yields a receptor variant that preferentially promotes STAT3/5 signaling. This STAT activation transcriptionally induces Grb14 in pancreatic endocrine cells to promote insulin secretion. Knockin mice with the FGFR4 variant allele develop pancreatic islets that secrete more insulin, a feature that is reversed through Grb14 deletion and enhanced with FGF19 administration. We also show in humans that the FGFR4-R388 allele enhances islet function and may protect against type 2 diabetes. These data support a common genetic link underlying cancer and hyperinsulinemia.
机译：成纤维细胞生长因子受体4（FGFR4）-R388单核苷酸多态性已与癌症风险和预后相关。在这里，我们显示FGFR4-R388等位基因产生优先促进STAT3 / 5信号转导的受体变体。 STAT的激活通过转录诱导胰腺内分泌细胞中的Grb14促进胰岛素分泌。具有FGFR4变异等位基因的敲除小鼠会发育出胰岛，该胰岛分泌更多的胰岛素，这一特征可通过Grb14缺失而逆转，并通过施用FGF19得以增强。我们还在人体中显示FGFR4-R388等位基因可增强胰岛功能，并可预防2型糖尿病。这些数据支持癌症和高胰岛素血症的常见遗传联系。

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