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

ABSTRACT: Single-cell RNA sequencing of pancreatic islets from 18-week-old male New Zealand Obese (NZO/HIBomDife) and B6.V-Lepob/ob (OB) mice were fed a standard diet or a carbohydrate-enriched diet for 2 additional days (+CH / -CH).

ORGANISM(S): Mus musculus

PROVIDER: GSE159211 | GEO | 2022/07/07

REPOSITORIES: GEO

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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.

2021-09-04 | GSE183247 | GEO

Gene expression in diabetes-prone (NZO/HiBomDife) and diabetes-resistant (C57BL/6.V-Lepob/ob) mouse strains

Project description:Mouse strains like NZO and B6-ob/ob differ in their susceptibility to diet-induced diabetes. Comparison of the islet transcriptomes leads to genes that are either involved in protection or apoptosis of pancreatic islet cells upon carbohydrate challenge. Genes being upregulated in NZO can be seen as drivers of beta cell failure, while genes upregulated in B6-ob/ob are most likely involved in beta cell protection.

2018-02-19 | GSE64956 | 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

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

miRNA sequencing profile of isolated Kit+ interstital cells of Cajal (ICC) in Leptin mutant mice

Project description:We report the high-throughput miRNA sequencing of isolated colonic and jejunal Kit+ interstitial cells of Cajal (ICC) from Lepob/ob;KitcopGFP mice, which develop type 2 diabetes, and Lepob/+;KitcopGFP mice which are non-diabetic counterparts and control

2020-12-31 | GSE139578 | GEO

Epigenetic changes in Langerhans islets preceding the onset of diabetes

Project description:Diabetes-resistant and diabetes-prone female New Zealand Obese mice were classified based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. By using transcriptome and DNA methylome analysis of Langerhans islets, we identified early epigenetic alteration in mice and humans which could serve as putative epigenetic biomarkers

2020-10-28 | GSE143875 | GEO

Transcriptome analysis of islets from diabetes-resistant and diabetes-prone obese mice reveals novel gene regulatory networks involved in beta cell compensation and failure

Project description:We carried out genome-wide transcriptome analysis of islets to investigate the gene expression landscape of ob/ob and db/db mouse models at 6 and 16 weeks of age. The purpose of this study is to determine the changes in the islet transcriptomic landscape that mediate the processes of beta cell compensation and failure in ob/ob and db/db mice.

2021-12-20 | GSE169275 | GEO

Genotype-by-diet interactions determine susceptibility and resistance in T2D mouse models [Islets 1]

Project description:Genetic and lifestyle factors greatly impact the development of metabolic diseases including Type 2 Diabetes (T2D). It is an ongoing challenge to determine how these factors and their interplay specifically contribute to risk of T2D. Mouse models allow precise control of environment and genetic replication, and mouse strains fed an unhealthy diet show variable signs of metabolic dysfunction ranging from overt diabetes to diet-induced obesity to complete resistance. When fed a high-fat high-sugar (HFHS) diet, NZO/HlLtJ (NZO) mice become severely obese and many become diabetic, C57BL/6J (B6J) mice develop obesity but seldom overt diabetes, and CAST/EiJ (CAST) mice are resistant to obesity and glucose intolerance. We present deep molecular and metabolic profiling of these three genetically diverse mouse strains fed control (low fat, no sugar) and HFHS diets to define inherited aspects of metabolism that may impact diabetes risk. Transcriptomic analysis of eight tissues revealed significant tissue-specific molecular variability underpinning the metabolic differences across strains. The most distinct diet responses were observed in adipose and pancreas. In adipose tissue, differences in immunometabolism, lipid metabolism, and oxidative phosphorylation pathways parallel the susceptibility to obesity and diabetes across strains. In pancreatic islets, there was inflammation associated with HFHS diet in NZO mice that is expected to contribute to beta cell dysfunction. Taken together, physiological and molecular profiling of these genetically diverse mouse strains provides a foundation for deeper understanding the molecular basis of individual differences in susceptibility to metabolic diseases.

2023-12-31 | GSE234956 | GEO

Enriched Alternative Splicing in Islets of Diabetes-Susceptible Mice.

Project description: Not available

| S-EPMC8395343 | biostudies-literature

Transcription profiling of adipose tissue, liver, skeletal muscle, and pancreatic islets from nondiabetic and diabetic obese mice to understand susceptibility to diabetes.

Project description:Obesity is a strong risk factor for the development of type 2 diabetes. We have previously reported that in adipose tissue of obese (ob/ob) mice, the expression of adipogenic genes is decreased. When made genetically obese, the BTBR mouse strain is diabetes susceptible and the C57BL/6J (B6) strain is diabetes resistant. We used DNA microarrays and RT-PCR to compare the gene expression in BTBR-ob/ob versus B6-ob/ob mice in adipose tissue, liver, skeletal muscle, and pancreatic islets. Our results show: 1) there is an increased expression of genes involved in inflammation in adipose tissue of diabetic mice; 2) lipogenic gene expression was lower in adipose tissue of diabetes-susceptible mice, and it continued to decrease with the development of diabetes, compared with diabetes-resistant obese mice; 3) hepatic expression of lipogenic enzymes was increased and the hepatic triglyceride content was greatly elevated in diabetes-resistant obese mice; 4) hepatic expression of gluconeogenic genes was suppressed at the prediabetic stage but not at the onset of diabetes; and 5) genes normally not expressed in skeletal muscle and pancreatic islets were expressed in these tissues in the diabetic mice. We propose that increased hepatic lipogenic capacity protects the B6-ob/ob mice from the development of type 2 diabetes. Diabetes 52:688â700, 2003 Experiment Overall Design: Four B6-ob/ob and four BTBR-ob/ob male mice at 14 weeks of age were used in the microarray study. RNA samples from two individuals were pooled for each tissue, and each pooled RNA sample was applied to an Affymetrix MGU74AV2 array. Because of the scarcity of islets in the BTBR-ob/ob mice, 4 additional mice were pooled to obtain islet RNA from these animals. Sixteen MGU74Av2 arrays (2 strains X 4 tissues X 2 replicates = 16 arrays) were used to monitor the expression level of â12,000 genes or ESTs.

2007-08-31 | E-GEOD-2899 | biostudies-arrayexpress

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