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Comparative assessment of the transcriptome of pancreatic islets from Non-Obese Diabetic mice in the absence of immune infiltrate

ABSTRACT: The transcriptome of pancreatic islets from four mouse strains was compared - NODk.RagKO, B10k.RagKO, NODk.RagKO.insHEL and B10k.RagKO.insHEL. This comparison allows the assessment of altered transcriptome due to two factors - genetic background of NOD vs B10 strain, and the effect of the insHEL transgene. The use of the MHC k haplotype and the RagKO background remove contamination from infiltrating immune cells, in order to obtain a pure islet transcriptome.

ORGANISM(S): Mus musculus

PROVIDER: GSE56507 | GEO | 2016/02/23

SECONDARY ACCESSION(S): PRJNA243560

REPOSITORIES: GEO

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Comparative assessment of the transcriptome of pancreatic islets from Non-Obese Diabetic mice in the absence of immune infiltrate

Project description:The transcriptome of pancreatic islets from four mouse strains was compared - NODk.RagKO, B10k.RagKO, NODk.RagKO.insHEL and B10k.RagKO.insHEL. This comparison allows the assessment of altered transcriptome due to two factors - genetic background of NOD vs B10 strain, and the effect of the insHEL transgene. The use of the MHC k haplotype and the RagKO background remove contamination from infiltrating immune cells, in order to obtain a pure islet transcriptome. Three mice of each gentoype were analyzed in this study.

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Project description:In insulin-resistant status such as obesity, failure of pancreatic islets to increase insulin secretion leads to diabetes. We sought to screen for the islet genes that facilitate islet adaptation to obesity by comparing gene expression profiles between two strains of obesity-prone inbred mice with different propensities for hyperglycemia. C57BL/6J and AKR/J were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function, and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57BL/6J mice on regular rodent chow or high-fat diet. Insulin secretion was 3.2-fold higher in AKR/J than C57BL/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4-fold greater in AKR/J compared with C57BL/6J. To elucidate the factors associated with the differences in islet function, we analyzed the gene expression profiles in islets in AKR/J and C57BL/6J mice. Of 14,000 genes examined, 202 were upregulated and 270 were downregulated in islets from diet-induced obese AKR/J mice compared with C57BL/6J mice. Key genes involved in islet signaling and metabolism, e.g., glucagon-like peptide-1 receptor, sterol Co-A desaturase 1 and 2, and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function.

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