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Transcription profiling of sorted beta cells from Liver-specific insulin receptor knock-out (LIRKO) mice

ABSTRACT: We investigated the transcriptomic make-up of a successful beta-cell compensation to insulin resistance. For this we sorted and performed mRNA-sequencing in FACS-sorted beta-cells from Control and LIRKO mice on Chow or a high-fat diet.

ORGANISM(S): Mus musculus

PROVIDER: GSE297142 | GEO | 2026/05/13

REPOSITORIES: GEO

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The hepatic transcriptome of liver-specific insulin receptor knockout (LIRKO) mouse offspring

Project description:At 2 months of age, liver-specific insulin receptor knockout (LIRKO) mice present hyperglycemia and hyperinsulinemia. Furthermore, LIRKO mice have increased levels of hepatic cholesterol. Indeed, many changes seen in cholesterol metabolism in LIRKO mice are also observed in humans with metabolic syndrome. For example, both show decreased levels of HDL and increased secretion of apoB and VLDL. These findings make the LIRKO mouse a unique non-dietary model of insulin resistant, hyperglycemia, dyslipidemia and atherosclerosis that resembles several clinical features of the human metabolic syndrome. By hepatic transcriptomic analysis of the wild-type (WT) offspring of LIRKO mice, we identify that members of the TGF-β family are differentially expressed in the offspring, including the NREP and GDF15.

2021-01-04 | GSE141077 | GEO

The hepatic methylome of liver-specific insulin receptor knockout (LIRKO) mouse offspring

Project description:Liver-specific insulin receptor knockout (LIRKO) mouse is a unique non-dietary model of insulin resistant, hyperglycemia, dyslipidemia and atherosclerosis that resembles several clinical features of the human metabolic syndrome. By enhanced reduced representation bisulfite sequencing (ERRBS) analysis of the livers of wild-type (WT) offspring of LIRKO mice, we identified that genes with differential DNA methylation were enriched for cholesterol synthesis, MAPK, AKT, insulin and TGF-β signaling, including the NREP and GDF15.

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m6A RIP-seq of beta-cell s from liver-specific insulin receptor knockout (LIRKO) mice

Project description:In type 2 diabetes, pancreatic beta-cells fail to compensate for the presence of insulin resistance in target tissues. Identifying and studying innovative molecular mechanisms that control the beta-cell adaptation to insulin resistance represent an interesting line of research and are necessary. N6-Methyladenosine (m6A) is the most abundant modification in mRNA and is found virtually in all mammals. Through m6A-profiling of Control and LIRKO islets we aimed to identify the m6A landscape of the successful beta-cell adaption to insulin resistance.

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Hepatic Gene Expression in LIRKO Mice

Project description:Control and Liver Insulin Receptor KO mice (LIRKO) were sacrificed in the non-fasted state. RNA was prepared from liver samples and subjected to expression microarray analysis Each array was hybridized with sample derived from 2-3 mice of the same genotype. Three arrays per group were used.

2015-02-05 | E-GEOD-65624 | biostudies-arrayexpress

Hepatic Gene Expression in LIRKO Mice

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Pancreatic beta cell proteome with increased proliferation in NOD mice

Project description:We investigated the pancreatic beta cell proteome changes in NOD-LIRKO vesus NOD where beta cell mass was enhanced early in life. Proteomics data is derived from FACS-sorted beta cells at 8 weeks and 12 weeks.

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The hepatic transcriptome of liver-specific insulin receptor knockout (LIRKO) mouse offspring

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Increased β-cell proliferation prior to immune-cell invasion prevents progression of type 1 diabetes

Project description:Type 1 diabetes (T1D) is characterized by pancreatic islet infiltration by autoreactive immune cells and a near-total loss of β-cells. Restoration of insulin-producing β-cells coupled with immunomodulation to suppress the autoimmune attack has emerged as a potential approach to counter T1D. Here we report that enhancing β-cell mass in female NOD mice early in life (prior to weaning) results in immunomodulation of T-cells, reduced islet infiltration and lower β-cell apoptosis, that together protect them from developing T1D. We observed that a model exhibiting β-cell hyperplasia on the NOD background (NOD-LIRKO) displayed altered β-cell antigens, and islet transplantation studies showed prolonged graft survival of NOD-LIRKO islets even upon exposure to diabetogenic splenocytes in vivo. Adoptive transfer of splenocytes from the NOD-LIRKOs prevented diabetes development in pre-diabetic NOD mice, while conversely, similar protective outcomes were obtained when NOD-LIRKO splenocytes were adoptively transferred after mixing them with diabetogenic NOD splenocytes in a dose-dependent manner. A significant increase in the splenic CD4+CD25+FoxP3+ regulatory T-cell (Treg) population in the NOD-LIRKO mice was observed to drive the protected phenotype since Treg depletion rendered NOD-LIRKO mice diabetic. The increase in Tregs coupled with a downregulation of key mediators of cellular function, upregulation of apoptosis and activation of TGF-β/SMAD3 signaling pathway in pathogenic T-cells favored reduced ability to kill β-cells. These data provide novel evidence that initiating β-cell proliferation, alone, prior to islet infiltration by immune cells alters the identity of β-cells, decreases pathologic self-reactivity of effector cells and increases Tregs to prevent progression of T1D.

2019-03-29 | GSE128315 | GEO

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