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Author Correction: Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure.

ABSTRACT:

SUBMITTER: Katz LS

PROVIDER: S-EPMC9515145 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

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Author Correction: Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure.

Katz Liora S LS Brill Gabriel G Zhang Pili P Kumar Anil A Baumel-Alterzon Sharon S Honig Lee B LB Gómez-Banoy Nicolás N Karakose Esra E Tanase Marius M Doridot Ludivine L Alvarsson Alexandra A Davenport Bennett B Wang Peng P Lambertini Luca L Stanley Sarah A SA Homann Dirk D Stewart Andrew F AF Lo James C JC Herman Mark A MA Garcia-Ocaña Adolfo A Scott Donald K DK

Nature communications 20220927 1

PMID: 36167859

Similar Datasets

Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure.

Project description:Preservation and expansion of β-cell mass is a therapeutic goal for diabetes. Here we show that the hyperactive isoform of carbohydrate response-element binding protein (ChREBPβ) is a nuclear effector of hyperglycemic stress occurring in β-cells in response to prolonged glucose exposure, high-fat diet, and diabetes. We show that transient positive feedback induction of ChREBPβ is necessary for adaptive β-cell expansion in response to metabolic challenges. Conversely, chronic excessive β-cell-specific overexpression of ChREBPβ results in loss of β-cell identity, apoptosis, loss of β-cell mass, and diabetes. Furthermore, β-cell "glucolipotoxicity" can be prevented by deletion of ChREBPβ. Moreover, ChREBPβ-mediated cell death is mitigated by overexpression of the alternate CHREBP gene product, ChREBPα, or by activation of the antioxidant Nrf2 pathway in rodent and human β-cells. We conclude that ChREBPβ, whether adaptive or maladaptive, is an important determinant of β-cell fate and a potential target for the preservation of β-cell mass in diabetes.

| S-EPMC9339008 | biostudies-literature

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.

2022-06-02 | GSE197864 | GEO

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

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