Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA256986 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mice were fasted for 18 hr overnight then sacrificed or treated with 13C-U-glucose (2 g/kg ip) and sacrificed 1 hr later by decapitation and liver was immediately freeze-clamped and stored in liquid N2 and then at -80 C. Wild type (IR and IR/FoxO1 floxed) mice were sacrificed after fasting and 1 hr post-glucose treatment. Liver-specific insulin receptor knockout (LIRKO) and insulin receptor/FoxO1 double knockout (LIRFKO) mice were sacrificed 1 hr post glucose treatment.
http://www.nature.com/ncomms/2015/150512/ncomms8079/full/ncomms8079.html
2015-06-12 | ST000215 | MetabolomicsWorkbench
Project description:FoxO proteins are major targets of insulin action. To better define the role of FoxO1 in mediating insulin effects in the liver, we generated liver-specific insulin receptor knockout (LIRKO) and IR/FoxO1 double knockout (LIRFKO) mice. Here we show that LIRKO mice are severely insulin resistant based on glucose, insulin and C-peptide levels, and glucose and insulin tolerance tests, and genetic deletion of hepatic FoxO1 reverses these effects. 13C-glucose and insulin clamp studies indicate that regulation of both hepatic glucose production (HGP) and glucose utilization is impaired in LIRKO mice, and these defects are also restored in LIRFKO mice corresponding to changes in gene expression. We conclude that (1) inhibition of FoxO1 is critical for both direct (hepatic) and indirect effects of insulin on HGP and utilization, and (2) extrahepatic effects of insulin are sufficient to maintain normal whole-body and hepatic glucose metabolism when liver FoxO1 activity is disrupted.
Research is published:
http://www.nature.com/ncomms/2015/150512/ncomms8079/full/ncomms8079.html
2015-06-10 | ST000198 | MetabolomicsWorkbench
Project description:The effect of liver specific deletion of the insulin receptor substrate-1 (Irs1) and/or Irs2 upon gene expression in the fasted and fed liver of mice; and the effect of liver specific Foxo1 deletion in the Irs1 and Irs2 knockout liver during fasting and feeding.
2008-07-31 | E-MEXP-1649 | biostudies-arrayexpress
Project description:Decreased skeletal muscle strength and mitochondrial dysfunction are characteristic of diabetes. Action of insulin through insulin receptor (IR) and IGF-1 receptor (IGF1R) maintain muscle mass via suppression of FoxOs, but whether FoxO activation coordinates atrophy in concert with mitochondrial dysfunction is unknown. In the absence of systemic glucose or lipid abnormalities, muscle-specific IR knockout (MIRKO) or combined IR/IGF1R knockout (MIGIRKO) impaired mitochondrial respiration, decreased ATP production, and increased ROS. These mitochondrial abnormalities were not present in muscle-specific IR/IGF1R and FoxO1/3/4 quintuple knockout mice (QKO). Although autophagy was increased when IR/IGF1R were deleted in muscle, mitophagy was not increased. Mechanistically, RNA-seq revealed that complex-I core subunits were decreased in MIGIRKO muscle, and these were reversed with FoxO knockout. Thus, insulin-deficient diabetes or loss of insulin/IGF-1 action in muscle decreases complex-I driven mitochondrial respiration and supercomplex assembly, in part by FoxO-mediated repression of Complex-I subunit expression.
2021-07-21 | GSE178356 | GEO
Project description:RNA-seq of livers in control and Cnot1 tamoxifen-inducible liver-specific knockout mice
2020-01-28 | E-MTAB-5901 | ExpressionAtlas
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:Expression data from macroH2A1/2 double knockout fetal mouse liver
2014-10-28 | E-GEOD-57086 | ExpressionAtlas
Project description:Transcriptional Profiling of Neuronal APP/APLP2 Double-Conditional Knockout Mice.
2015-07-16 | E-GEOD-48622 | ExpressionAtlas
Project description:Liver gene expression from chromogranin A knockout mice (Mahapatra et al. 2005) vs. wild-type mice
2014-07-03 | E-GEOD-18305 | ExpressionAtlas
Project description:Transcription profiling by array of pancreatic islets from pancreas-specific Hnf4alpha knockout, heterozygous Hnf1alpha, and double mutant mice
2014-07-08 | E-MEXP-1729 | ExpressionAtlas