Gpr27 is a highly conserved, orphan G protein coupled receptor (GPCR) previously implicated in pancreatic beta cell insulin transcription and glucose-stimulated insulin secretion in vitro. Here, we characterize a whole-body mouse knockout of Gpr27. Gpr27 knockout mice were born at expected Mendelian ratios and exhibited no gross abnormalities. Insulin and Pdx1 mRNA in Gpr27 knockout islets were reduced by 30%, but this did not translate to a reduction in islet insulin content or beta cell mass. Gpr27 knockout mice exhibited slightly worsened glucose tolerance with lower plasma insulin levels while maintaining similar insulin tolerance. Unexpectedly, Gpr27 deletion reduced expression of Eif4e3, a neighboring gene, likely by deleting transcription start sites on the anti-sense strand of the Gpr27 coding exon. Our data confirm that loss of Gpr27 reduces insulin mRNA in vivo but has only minor effects on glucose tolerance.

Gpr27是一种高度保守的孤儿 G 蛋白偶联受体 (GPCR)，之前在体外与胰腺 β 细胞胰岛素转录和葡萄糖刺激的胰岛素分泌有关。在这里，我们描述了Gpr27的全身小鼠敲除。 Gpr27基因敲除小鼠以预期的孟德尔比率出生，并且没有表现出明显的异常。 Gpr27敲除胰岛中的胰岛素和Pdx1 mRNA 减少了 30%，但这并不意味着胰岛胰岛素含量或 β 细胞质量的减少。 Gpr27敲除小鼠表现出稍微恶化的葡萄糖耐量，血浆胰岛素水平较低，同时保持相似的胰岛素耐量。出乎意料的是， Gpr27缺失可能通过删除Gpr27编码外显子反义链上的转录起始位点来减少邻近基因Eif4e3的表达。我们的数据证实， Gpr27的缺失会减少体内胰岛素 mRNA，但对葡萄糖耐量的影响很小。