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Induction of alpha cell-restricted Gc in dedifferentiating beta cells contributes to stress-induced beta-cell dysfunction [ChIP-seq]

ABSTRACT: Induction of alpha cell-restricted Gc in dedifferentiating beta cells contributes to stress-induced beta-cell dysfunction [ChIP-seq]

PROVIDER: PRJNA542265 | ENA |

REPOSITORIES: ENA

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Induction of alpha cell-restricted Gc in dedifferentiating beta cells contributes to stress-induced beta-cell dysfunction [RNA-seq]

Project description:Induction of alpha cell-restricted Gc in dedifferentiating beta cells contributes to stress-induced beta-cell dysfunction [RNA-seq]

| PRJNA542266 | ENA

Induction of alpha cell-restricted Gc in dedifferentiating beta cells contributes to stress-induced beta-cell dysfunction [RNA-seq]

Project description:To identify effector genes of pancreatic beta cell dedifferentiation and dysfunction, we performed RNA expression in beta cells sorted from mice with multiparity-induced diabetes.

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Induction of alpha cell-restricted Gc in dedifferentiating beta cells contributes to stress-induced beta-cell dysfunction [ChIP-seq]

Project description:To identify effector genes of pancreatic beta cell dedifferentiation and dysfunction, we integrated analyses of histone methylation as a surrogate of gene activation status and RNA expression in beta cells sorted from mice with multiparity-induced diabetes.

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Induction of α cell-restricted Gc in dedifferentiating β cells contributes to stress-induced β-cell dysfunction.

Project description: Not available

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Time-restricted feeding prevents deleterious metabolic effects of circadian disruption through epigenetic control of β-cell function [ATACseq]

Project description:Circadian rhythm disruption (CD) is associated with dysregulation of glucose homeostasis and Type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates CD-induced metabolic dysfunction. Herein we utilized an approach encompassing analysis of behavioral, physiological, transcriptomic, and single-cell epigenomic effects of CD and consequences of restoration of fasting/feeding cycles through time-restricted feeding (tRF) in mice. Results show that CD perturbs glucose homeostasis through disruption of pancreatic β-cell function and loss of circadian β-cell transcriptional and epigenetic control. In contrast, restoration of fasting/feeding cycle prevented CD-mediated metabolic dysfunction by reestablishing circadian regulation of glucose tolerance, β-cell function, β-cell transcriptional profile, and reestablishment of proline and acidic amino acid-rich basic leucine zipper (PAR-bZIP) transcription factor activity in β-cells. This study provides mechanistic insights into beneficial effects of tRF and its role in prevention of β-cell failure in T2DM.

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Endoplasmic reticulum stress leads to pancreatic beta-cell desensitization to incretin and beta-cell dysfunction via ATF4-mediated PDE4D expression

Project description:Pancreatic beta-cell dysfunction and eventual beta-cell loss are key steps in the course of type 2 diabetes (T2D). Endoplasmic reticulum (ER) stress, in particular the PERK-ATF4 pathway, has been implicated in promoting these beta-cell pathologies. However, the exact molecular events surrounding the PERK-ATF4 pathway in beta-cell dysfunction remain unknown. Here, we discovered that ATF4 transcriptionally promotes expression of PDE4D, which results in beta-cell dysfunction via downregulation of cAMP signaling. Beta-cell-specific transgenic expression of ATF4 resulted in early beta-cell dysfunction and loss, resembling accelerated T2D. ATF4 expression, rather than CHOP, promoted PDE4D expression, decreased cAMP signaling, and attenuated responses to incretins and elevated glucose. Further, beta-cells of leptin receptor-deficient diabetic (db/db) mice expressed increased levels of ATF4 and PDE4D, accompanying impaired beta-cell function. Moreover, inhibiting PDE4D activity with selective pharmacological inhibitors significantly ameliorated beta-cell dysfunction in both db/db mice and beta-cell-specific ATF4 transgenic mice. In summary, our findings support that ER stress causes beta-cell failure via ATF4-mediated PDE4D production, and this is a highly promising therapeutic target for protecting beta-cell function during progression of T2D.

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miR-146a-5p contributes to inflammation-mediated β cell mitochondrial dysfunction and apoptosis

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2024-04-10 | GSE255756 | GEO

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