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The impact of aging on beta-cell functionality and structural integrity under metabolic stress conditions in diabetes-prone and diabetes-resistant mice.

ABSTRACT: The impact of aging on beta-cell functionality and structural integrity under metabolic stress conditions in diabetes-prone and diabetes-resistant mice.

PROVIDER: PRJNA631714 | ENA |

REPOSITORIES: ENA

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The impact of aging on beta-cell functionality and structural integrity under metabolic stress conditions in diabetes-prone and diabetes-resistant mice [ob].

Project description:The impact of aging on beta-cell functionality and structural integrity under metabolic stress conditions in diabetes-prone and diabetes-resistant mice [ob].

| PRJNA674026 | ENA

The impact of aging on beta-cell functionality and structural integrity under metabolic stress conditions in diabetes-prone and diabetes-resistant mice.

Project description:Overnutrition contributes to insulin resistance, obesity and metabolic stress, initiating a loss of functional beta-cells and diabetes development. Whether these damaging effects are amplified in advanced age is barely investigated. Therefore, New Zealand Obese (NZO) mice, a well-established model for the investigation of human obesity-associated type 2 diabetes, were fed a metabolically challenging diet with a high-fat, carbohydrate restricted period followed by a carbohydrate intervention in young as well as advanced age. Interestingly, while young NZO mice developed massive hyperglycemia in response to carbohydrate feeding, leading to beta-cell dysfunction and cell death, aged counterparts compensated the increased insulin demand by persistent beta-cell function and beta-cell mass expansion. Beta-cell loss in young NZO islets was linked to increased expression of thioredoxin-interacting protein (TXNIP), presumably initiating an apoptosis-signaling cascade via caspase-3 activation. In contrast, islets of aged NZOs exhibited a sustained redox balance without changes in TXNIP expression, associated with higher proliferative potential by cell cycle activation. These findings support the relevance of a maintained proliferative potential and redox homeostasis for preserving islet functionality under metabolic stress, with the peculiarity that this adaptive response emerged with advanced age in diabetes-prone NZO mice.

2020-11-02 | GSE150281 | GEO

The impact of aging on beta-cell functionality and structural integrity under metabolic stress conditions in diabetes-prone and diabetes-resistant mice [ob].

Project description:Young and aged, diabetes-prone (NZO/HIBomDife) as well as diabetes-resistant (B6.V-Lep ob/ob) mice exhibited different islet functions and phenotypes in response to a carbohydrate-rich diet (CRD) subsequent to a high-fat, carbohydrate-free diet (HFD). To unravel the molecular basis underlying these alterations, a microarray-based transcriptome analysis of isolated pancreatic islets before and after 2 days of CRD feeding was performed. A high number of differentially expressed genes associated with redox homeostasis, in particular Thioredoxin-interacting protein (Txnip), as well as genes involved in cell cycle entry and cell proliferation, such as cyclins, cyclin-dependent kinases and Mki67 were identified and associated with these changes. In addition, aged NZO/HIBomDife and age-matched, B6.V-Lep ob/ob mice revealed a high overlap of regulated genes, also linked to cell cycle progression under the same dietary regimen.

2023-11-03 | GSE160694 | GEO

Pancreatic Differentiation of stem cells reveals pathogenesis of a syndrome of Ketosis-Prone Diabetes

Project description:We describe an unusual course of Ketosis Prone Diabetes and investigate potential mechanisms using induced pluripotent stem cell technology with high throughput mRNA sequencing and validation of a lecuine sensitive mTOR pathway.

2021-06-01 | GSE165385 | GEO

β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [CUT&RUN]

Project description:Replication stress is a main driver of functional decline of hematopoietic stem cells (HSCs), which carry the highest burden of maintaining genomic integrity and functionality within the hematopoietic system. Here, we identify a novel signaling axis in which β-catenin and Hoxa9 function in a compensatory manner to preserve HSC functionality by protecting DNA replication dynamics and genomic integrity, in part via regulation of Prmt1 activity. Co-inactivation of β-catenin and Hoxa9 induces severe hematopoietic defects accompanied by accumulating replication stress and DNA damage resulting in functional HSC decline. Furthermore, we illustrate how β-catenin and Hoxa9 pathways converge on the pivotal downstream target, Prmt1, which functions to maintain an adequate supply of DNA replication and repair factors. Prmt1 aids in alleviating replication stress and DNA damage accumulation thereby preserving HSC integrity and functionality.

2024-02-29 | GSE249199 | GEO

β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [ATAC-Seq]

2024-02-29 | GSE235815 | GEO

β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq LSK]

2024-02-29 | GSE235816 | GEO

β-catenin and Hoxa9 preserve DNA replication dynamics, genomic integrity and stem cell functionality in a Prmt1-dependent manner [RNA-seq dKO_HSPCs]

2024-02-29 | GSE235817 | GEO

Pancreatic Differentiation of stem cells reveals pathogenesis of a syndrome of Ketosis-Prone Diabetes

Project description:Pancreatic Differentiation of stem cells reveals pathogenesis of a syndrome of Ketosis-Prone Diabetes

| PRJNA694301 | ENA

The repertoire of newly developing regulatory T cells in the type I diabetes-prone NOD mouse is very diverse

Project description:Regulatory T lymphocytes expressing the forkhead/winged helix transcription factor Foxp3 (Treg) play a vital role in the protection of the organism from autoimmune disease and other immunopathologies. The antigen-specificity of Treg plays an important role in their in vivo activity. We therefore assessed the diversity of the T cell receptors for antigen (TCR) expressed by Treg newly developed in the thymus of autoimmune type I diabetes-prone NOD mice and compared it to the control mouse strain C57BL/6. Our results demonstrate that usage of the TCRα and TCRβ variable (V) and joining (J) segments, length of the complementarity determining region (CDR) 3, and the diversity of the TCRα and TCRβ chains are comparable between NOD and C57BL/6 mice. Genetic defects affecting the diversity of the TCR expressed by newly developed Treg therefore do not appear to be involved in the etiology of type I diabetes in the NOD mouse.

2021-05-31 | GSE159001 | GEO

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