Abstract
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.
Highlights
Gpr[27] 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
We previously identified the highly conserved GPCR Gpr[27] as a positive regulator of both insulin transcription and insulin secretion during a loss of function screen conducted in the MIN6 pancreatic beta cell line[5]
To explore the role of Gpr[27] in glucose homeostasis in vivo, we studied a whole body Gpr[27] knockout mouse
Summary
Gpr[27] 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. We previously identified the highly conserved GPCR Gpr[27] ( known as SREB1, or super conserved receptor in brain 1) as a positive regulator of both insulin transcription and insulin secretion during a loss of function screen conducted in the MIN6 pancreatic beta cell line[5]. Gpr[27] is predominantly expressed in the brain, pituitary, and the pancreatic beta cell[5] (GTEx Portal) While this previous work indicates that Gpr[27] may represent a new therapeutic target for diabetes, Gpr[27] remains uncharacterized in vivo. Gpr[27] knockout mice had reduced body mass, had modest worsening of glucose intolerance, and had decreased plasma insulin levels. This work adds to our understanding of the role of Gpr[27] in regulating glucose homeostasis in vivo
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