Gut microorganisms in insulin-resistant mice
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PROVIDER: PRJEB90460 | ENA |
REPOSITORIES: ENA
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Project description:Rosuvastatin ameliorates obesity-associated insulin resistance in high-fat diet-fed mice by modulating the gut microbiota.
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Project description:Male C57BL/6J mice were fed a high-fat diet (HFD, 60 kcal% fat, D12492, Research Diets, Inc) or normal standard chow diet with 10 kal% fat (ND, D09100304, Research Diets, Inc). Specifically, 6-week-old mice were fed a HFD for 12 weeks to induce insulin resistance (HFD-12w group); 14-week-old mice were fed a HFD for 4 weeks to induce obesity (HFD-4w group). Control mice were fed a ND continuously for 12 weeks starting at 6 weeks of age (ND group). All mice reached the experimental endpoint at 18 weeks of age. Insulin sensitivity was measured by glucose tolerance test and insulin tolerance test. Mice that developed insulin resistance in HFD-12w group and obese mice with normal insulin sensitivity in HFD-4w group were used for further experiments. Mice in ND group were used as controls. Upon reaching the experimental endpoint, livers from three insulin-resistant mice, three insulin-sensitive obese mice, and three control mice were removed for RNA sequencing.
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2015-04-25 | E-GEOD-68225 | biostudies-arrayexpress
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2022-06-01 | GSE147562 | GEO
Project description:The current study aimed to address the hypothesis that programmed expression of key miRNAs in skeletal muscle mediates the development of insulin resistance, and consequently long-term health. We thus examined microRNA signatures in skeletal muscle of programmed insulin resistant rats offspring from high fat-fed dams vs control offspring from chow fed dams.
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Project description:We developed a novel network inference approach, Biologically Anchored Knowledge Expansion (BAKE), to analyze large volume gene expression data obtained from a mouse model of insulin resistance progression. Both genetic aspects and dietary factors, specifically high caloric high-fat high-sugar diets, contribute to the progression of insulin resistance. To mimic genetic predisposition, we used a mouse model with double heterozygous deletion of early insulin signaling pathway intermediates, insulin receptor (IR) and insulin receptor substrate 1 (IRS1) genes. These mice were fed with high-fat (Western) or low-fat (Chow) diet for 8 and 16 weeks starting at 8 weeks of age. Gene expression data was collected from adipocytes isolated from these mice. Applying BAKE analysis to the adipocyte gene expression data, we demonstrate that we can accurately discover a novel regulatory gene in the insulin signaling pathway. The mouse model of double heterozygous deletion of insulin receptor (IR) and insulin receptor substrate 1 (IRS1) was originally introduced as a polygenic model to study the development of type 2 diabetes. This mouse model, on an atherosclerosis-prone ApoE null background (IR+/- IRS1+/- ApoE-/-), also shows increased atherosclerotic lesions due to impaired insulin signaling. For our study we used female double heterozygous mice (IR+/- IRS1+/-, 'Dhet' mice or 'Dâ mice) on an ApoE null background (ApoE-/-, âEâ) fed with a Western (high-fat) diet for 8 (DW8, n=5) and 16 (DW16, n=9) weeks starting at 8 weeks of age or with a Chow (low-fat) diet (DC8, n=7; DC16, n=5). There were also ApoE null mice (ApoE-/-, 'Eâ) fed either Western diet for 8 (EW8, n=6) and 16 (EW16, n=8) weeks or Chow diet for 16 weeks (EC16, n=5) starting at 8 weeks of age.
2015-12-31 | E-GEOD-76428 | biostudies-arrayexpress
Project description:We developed a novel network inference approach, Biologically Anchored Knowledge Expansion (BAKE), to analyze large volume gene expression data obtained from a mouse model of insulin resistance progression. Both genetic aspects and dietary factors, specifically high caloric high-fat high-sugar diets, contribute to the progression of insulin resistance. To mimic genetic predisposition, we used a mouse model with double heterozygous deletion of early insulin signaling pathway intermediates, insulin receptor (IR) and insulin receptor substrate 1 (IRS1) genes. These mice were fed with high-fat (Western) or low-fat (Chow) diet for 8 and 16 weeks starting at 8 weeks of age. Gene expression data was collected from adipocytes isolated from these mice. Applying BAKE analysis to the adipocyte gene expression data, we demonstrate that we can accurately discover a novel regulatory gene in the insulin signaling pathway.
2015-12-31 | GSE76428 | GEO
Project description:Folic acid (FA) supplementation may protect from obesity and insulin resistance, the effects and mechanism of FA on chronic high-fat-diet-induced obesity-related metabolic disorders are not well elucidated. We adopted a genome-wide approach to directly examine whether FA supplementation affects the DNA methylation profile of mouse adipose tissue and identify the functional consequences of these changes. Mice were fed a high-fat diet (HFD), normal diet (ND) or an HFD supplemented with folic acid (20 μg/ml in drinking water) for 10 weeks, epididymal fat was harvested, and genome-wide DNA methylation analyses were performed using methylated DNA immunoprecipitation sequencing (MeDIP-seq). Mice exposed to the HFD expanded their adipose mass, which was accompanied by a significant increase in circulating glucose and insulin levels. FA supplementation reduced the fat mass and serum glucose levels and improved insulin resistance in HFD-fed mice. MeDIP-seq revealed distribution of differentially methylated regions (DMRs) throughout the adipocyte genome, with more hypermethylated regions in HFD mice. Methylome profiling identified DMRs associated with 3787 annotated genes from HFD mice in response to FA supplementation. Pathway analyses showed novel DNA methylation changes in adipose genes associated with insulin secretion, pancreatic secretion and type 2 diabetes. The differential DNA methylation corresponded to changes in the adipose tissue gene expression of Adcy3 and Rapgef4 in mice exposed to a diet containing FA. FA supplementation improved insulin resistance, decreased the fat mass, and induced DNA methylation and gene expression changes in genes associated with obesity and insulin secretion in obese mice fed a HFD.
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