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FFAR3 modulates insulin secretion and global gene expression in mouse islets

机译：FFAR3调节小鼠胰岛中的胰岛素分泌和全局基因表达

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The short chain fatty acid (SCFA) receptor (free fatty acid receptor-3; FFAR3) is expressed in pancreatic cells; however, its role in insulin secretion is not clearly defined. Here, we examined the role of FFAR3 in insulin secretion. Using islets from global knockout FFAR3 (Ffar3(-/-)) mice, we explored the role of FFAR3 and ligand-induced FFAR3 signaling on glucose stimulated insulin secretion. RNA sequencing was also performed to gain greater insight into the impact of FFAR3 deletion on the islet transcriptome. First exploring insulin secretion, it was determined that Ffar3(-/-) islets secrete more insulin in a glucose-dependent manner as compared to wildtype (WT) islets. Next, exploring its primary endogenous ligand, propionate, and a specific agonist for FFAR3, signaling by FFAR3 inhibited glucose-dependent insulin secretion, which occurred through a G(i/o) pathway. To help understand these results, transcriptome analyses by RNA-sequencing of Ffar3(-/-) and WT islets observed multiple genes with well-known roles in islet biology to be altered by genetic knockout of FFAR3. Our data shows that FFAR3 signaling mediates glucose stimulated insulin secretion through G(i/o) sensitive pathway. Future studies are needed to more rigorously define the role of FFAR3 by in vivo approaches.
机译：短链脂肪酸（SCFA）受体（游离脂肪酸受体3; FFAR3）在胰腺细胞中表达;但是，其在胰岛素分泌中的作用尚不清楚。在这里，我们检查了FFAR3在胰岛素分泌中的作用。使用来自全球敲除FFAR3（Ffar3（-/-））小鼠的胰岛，我们探索了FFAR3和配体诱导的FFAR3信号转导对葡萄糖刺激的胰岛素分泌的作用。还进行了RNA测序，以更深入地了解FFAR3缺失对胰岛转录组的影响。首先探索胰岛素分泌，已确定与野生型（WT）胰岛相比，Ffar3（-/-）胰岛以葡萄糖依赖性方式分泌更多的胰岛素。接下来，探索其主要的内源性配体，丙酸酯和FFAR3的特异性激动剂，通过FFAR3进行的信号传导抑制了葡萄糖依赖性胰岛素的分泌，这是通过G（i / o）途径发生的。为了帮助理解这些结果，通过Ffar3（-/-）和WT胰岛的RNA测序进行转录组分析，观察到在胰岛生物学中具有众所周知作用的多个基因会因基因敲除FFAR3而改变。我们的数据表明，FFAR3信号通过G（i / o）敏感途径介导葡萄糖刺激的胰岛素分泌。需要进一步的研究以通过体内方法更严格地定义FFAR3的作用。

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