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Transcriptomic analyses of ChREBPtotal-null mice and ChREBPβ-null mice perigonadal white adipose tissue

ABSTRACT: The Carbohydrate Responive Element Binding Protein (ChREBP) is a transcription factor sensing glucose. Two isoforms are produced by the same gene, the long isoform ChREBPalpha and the short one ChREBPbeta transcribed from an alternative promoter. ChREBPalpha activates transcription of ChREBPbeta in response to glucose. The latter is thought to mediate most of the ChREBP transcriptional activation of target genes. However, the contribution of ChREBPbeta in metabolic adaptations in vivo is not known. This study aims at dertermining the contribution of the short isoform ChREBPbeta to the changes in gene expression mediated by ChREBP.

ORGANISM(S): Mus musculus

PROVIDER: GSE179562 | GEO | 2024/07/04

REPOSITORIES: GEO

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Transcriptomic analyses of ChREBPtotal-null mice and ChREBPβ-null mice liver

Project description:The Carbohydrate Responive Element Binding Protein (ChREBP) is a transcription factor sensing glucose. Two isoforms are produced by the same gene, the long isoform ChREBPalpha and the short one ChREBPbeta transcribed from an alternative promoter. ChREBPalpha activates transcription of ChREBPbeta in response to glucose. The latter is thought to mediate most of the ChREBP transcriptional activation of target genes. However, the contribution of ChREBPbeta in metabolic adaptations in vivo is not known. This study aims at dertermining the contribution of the short isoform ChREBPbeta to the changes in gene expression mediated by ChREBP.

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Maladaptive Positive Feedback Production of ChREBPβ Drives Glucotoxic β-Cell Failure

Project description:Purpose: Test the role of ChREBPbeta in pancreatic beta cells using tools that distinguish ChREBPalpha and ChREBPbeta and loss and gain of function experiments, confirming its role in glucose toxicity and finding mitigation strategies. Methods: INS-1 832/13 cells cultured in 2 mM or 11 mM glucose were transduced with adenoviruses expressing GFP as control or ChREBPbeta. After 48 h, RNA was isolated and amplified via the NuGEN Ovation RNA-Seq System V2 prior to RNA sequencing. Human islets from non-diabetic and T2D subjects were transduced with adenovirus ZSGreen and cell sorted. RNA was isolated and subjected to RNAseq. Results: Overexpression of ChREBPbeta led to increased expression of cell cycle and apoptotic genes and a decrease in beta cell maturity genes. T2D human beta cells expressed an increased ratio of ChREBPbeta to ChREBPalpha compared to non-diabetics. Conclusions: ChREBPbeta is necessary for adaptive beta cell expansion, but drives glucose toxicity when overexpressed, mimicking the graded effect of Myc overexpression in beta cells.

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