Litcius/Paper detail

Deletion of Gpr27 in vivo reduces insulin mRNA but does not result in diabetes

Deeksha Gambhir Chopra, Nicholas Yiv, Thomas G. Hennings, Yaohuan Zhang, Gregory Ku

2020Scientific Reports20 citationsDOIOpen Access PDF

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.

Topics & Concepts

PDX1InsulinEndocrinologyInternal medicineBeta cellBiologyIsletKnockout mouseIn vivoDiabetes mellitusMessenger RNAExonPancreatic isletsInsulin receptorGlucose tolerance testReceptorGeneInsulin resistanceMedicineGeneticsPancreatic function and diabetesReceptor Mechanisms and SignalingDiabetes Treatment and Management