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Gene expression signatures between lean and diabetes resistant B6 and 129/Ola, diabetes susceptible DBA and C3H mice and obese and diabetes susceptible NZO mice

ABSTRACT: Gene expression signatures between lean and diabetes resistant B6 and 129/Ola, diabetes susceptible DBA and C3H mice and obese and diabetes susceptible NZO mice

PROVIDER: PRJNA611766 | ENA |

REPOSITORIES: ENA

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Gene expression signatures between lean and diabetes resistant B6 mice and obese and diabetes susceptible NZO mice.

Project description:Gene expression signatures between lean and diabetes resistant B6 mice and obese and diabetes susceptible NZO mice.

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Gene expression signatures between lean and diabetes resistant B6 mice and obese and diabetes susceptible NZO mice. [ liver]

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Gene expression signatures between lean and diabetes resistant B6 and 129/Ola, diabetes susceptible DBA and C3H mice and obese and diabetes susceptible NZO mice

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Enriched Alternative Splicing in Islets of Diabetes-Susceptible Mice

Project description:Mouse strains like NZO and B6-ob/ob differ in their susceptibility to diet-induced diabetes. Comparison of the islet transcriptomes already revealed different biological processes, here we focused on alternative splicing events as one possible mechanism.

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Gene expression signatures between lean and diabetes resistant B6 mice and obese and diabetes susceptible NZO mice.

Project description:Whole genome microarray expression was measured in metabolic active tissues (gonadal white adipose tissue, brown adipose tissue and skeletal muscle) of 6 week old mice to detect changes in gene expression related to early onset of diabetes and obesity.

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Project description:Whole genome microarray expression was measured in liver tissue of 6 week old mice to detect changes in gene expression related to early onset of diabetes and obesity.

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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.

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.

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Single-cell RNA sequencing of pancreatic islets from obese mice with different diabetes risk reveals diabetes-susceptible β cell clusters

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2022-07-07 | GSE159211 | GEO

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