Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA312820 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The genomic analysis of liver from mice fed with standard or methyl and choline deficient (MCD) diet and treated with dual agonist of GLP1R/GCGR during two weeks before 70% partial hepatectomy (PH) and after 2 weeks PH resulted in a set of genes regulated by diet and other set regulated differentially by treatment in MCD treated animals. These genes are apparently responsible for the reversion and prevention of NAS and improvement in hepatic regeneration induced by drug treatment All microarray analyses were performed with RNA samples obtained from four independent liver from animals with different diet and drug treatmens.
2016-02-23 | E-GEOD-78170 | biostudies-arrayexpress
Project description:The genomic analysis of liver from mice fed with standard or methyl and choline deficient (MCD) diet and treated with dual agonist of GLP1R/GCGR during two weeks before 70% partial hepatectomy (PH) and after 2 weeks PH resulted in a set of genes regulated by diet and other set regulated differentially by treatment in MCD treated animals. These genes are apparently responsible for the reversion and prevention of NAS and improvement in hepatic regeneration induced by drug treatment
2016-02-23 | GSE78170 | GEO
Project description:Co-agonists at the glucagon-like peptide-1/glucagon receptors (GLP1R/GCGR) show promise as treatments for metabolic dysfunction-associated steatotic liver disease (MASLD). Unlike GLP1, glucagon directly acts on the liver to reduce fat content. To date most metabolic studies have looked at heavily GLP1R-biased co-agonists and have not distinguished weight-loss versus weight loss-independent effects. We demonstrate that 24 days’ treatment with Dicretin, a GLP1/GCGR co-agonist with high potency at the GCGR, in mice with hepatic steatosis secondary to diet-induced obesity leads to superior reduction of hepatic lipid content when compared to Semaglutide or equivalent weight loss by calorie restriction. Hepatic transcriptomic and metabolomic profiling demonstrated many changes that were unique to Dicretin-treated mice: some known targets of glucagon signalling and others with as yet unclear physiological significance. Our study supports the development of GLP1/GCGR co-agonists for treatment of MASLD and related conditions.
2024-06-11 | GSE243681 | GEO
Project description:The genomic analysis of liver from mice fed with standard or MCD diet and treated with FC-GLP-1 during two weeks before 70%partial hepatectomy (PH) and after 2 weeks PH resulted in a set of genes regulated by diet and other set regulated differentially by treatment in MCD treated animals. These genes are apparently responsible for the reversion and prevention of NAS and improvement in hepatic regeneration induced by drug treatment
2018-09-11 | GSE119725 | GEO
Project description:Glucagon and glucagon-like peptide-1 (GLP-1) are hormones involved in energy homeostasis. GLP-1 receptor (GLP-1R) agonism reduces food intake and delays gastric emptying, and glucagon receptor (GCGR) agonism increases energy expenditure by thermogenesis. BI 456906 is a subcutaneous, once-weekly injectable dual GLP-1R/GCGR agonist in development for the treatment of obesity or non-alcoholic steatohepatitis. Here we show that BI 456906 is a potent dual agonist with an extended half-life in human plasma. Key GLP-1R-mediated mechanisms of reduced food intake, delayed gastric emptying and improved glucose tolerance were confirmed in GLP-1R knockout mice. GCGR activity was confirmed by reduced plasma amino acids, increased hepatic expression of nicotinamide N-methyltransferase and increased energy expenditure. BI 456906 produced greater bodyweight reductions than maximally efficacious semaglutide doses and modulated gene expression, including genes involved in amino acid metabolism. BI 456906 is a potent dual agonist that produces bodyweight-lowering effects through both GLP-1R and GCGR agonism.
2022-12-09 | GSE211105 | GEO
Project description:It is known that administration of MCD induces a severe state of hepatic fibrosis in mice. To attempt to elucidate molecular mechanism of hepatic fibrosis, we performed whole transcriptome analysis by microarray using RNAs prepared from liver of wild-type mice fed with normal diet (ND) or MCD.
2023-12-06 | GSE249485 | GEO
Project description:It is known that administration of MCD induces a severe state of hepatic fibrosis in mice. Recently, many microRNAs (miRNAs) with pro- or anti-fibrotic properties have been identified during hepatic fibrosis. To attempt to elucidate molecular mechanism of hepatic fibrosis involved in miRNA fnction, we performed comprehensive analysis of miRNA expression by microarray using RNAs prepared from liver of wild-type mice fed with normal diet (ND) or MCD.
2023-12-06 | GSE249486 | GEO
Project description:Glucagon, an essential regulator of glucose and lipid metabolism, also promotes weight loss, in part through potentiation of fibroblast-growth factor 21 (FGF21) secretion. However, FGF21 is only a partial mediator of metabolic actions ensuing from GcgR-activation, prompting us to search for additional pathways. Intriguingly, chronic GcgR agonism increases plasma bile acid levels. We hypothesized that GcgR agonism regulates energy metabolism, at least in part, through farnesoid X receptor (FXR). To test this hypothesis, we studied whole body and liver-specific FXR knockout (FXR∆liver) mice. Chronic GcgR agonist (IUB288) administration in diet-induced obese (DIO) Gcgr, Fgf21 and Fxr whole body or liver-specific knockout (∆liver) mice failed to reduce body weight (BW) when compared to wildtype (WT) mice. IUB288 increased energy expenditure and respiration in DIO WT mice, but not FXR∆liver mice. GcgR agonism increased [14C]-palmitate oxidation in hepatocytes isolated from WT mice in a dose-dependent manner, an effect blunted in hepatocytes from FXR∆liver mice. Our data clearly demonstrate that control of whole body energy expenditure by GcgR agonism requires intact FXR signaling in the liver. This heretofore-unappreciated aspect of glucagon biology has implications for the use of GcgR agonism in the therapy of metabolic disorders.
2019-08-16 | GSE135881 | GEO
Project description:We performed survival analysis of control and MCD groups, and explored underlying tumor suppression mechanisms after dietary intervention, focused on alterations in the energy-dependent signaling pathways, histone modifications, and global gene expression differences on cDNA microarray study. Illumina arrays: Five- week- old male C57BL6 mice were randomly divided into two groups and fed control diet (control group, LabDiet, Brentwood, MO, USA) or moderate restriced carbohydrate diet formula (MCD, Treat group) in a specific pathogen free zone. All procedures were approved by the institutional animal use and care committee. Following a preliminary feeding of each diet formula for one week, 1 × 106 B16F10 cells (suspended with 100 μl of PBS) were subcutaneously injected into the back of the mice. After 2 weeks of diet supplementation, all mice were sacrificed. Tumor tissue was excised for cDNA microarray. Agilent arrays: Five- week- old male C57BL6 mice were randomly divided into two groups and fed control diet (control group, LabDiet, Brentwood, MO, USA) or moderate restriced carbohydrate diet formula (MCD, Treat group) in a specific pathogen free zone. All procedures were approved by the institutional animal use and care committee. Following a preliminary feeding of each diet formula for one week, 1 × 106 B16F10 cells (suspended with 100 μl of PBS) were subcutaneously injected into the back of the mice. After 2 weeks of diet supplementation, all mice were sacrificed. Tumor tissue was excised for chip-on-chip microarray.
2012-03-21 | E-GEOD-36633 | biostudies-arrayexpress
Project description:We performed survival analysis of control and MCD groups, and explored underlying tumor suppression mechanisms after dietary intervention, focused on alterations in the energy-dependent signaling pathways, histone modifications, and global gene expression differences on cDNA microarray study. Five- week- old male C57BL6 mice were randomly divided into two groups and fed control diet (control group, LabDiet, Brentwood, MO, USA) or moderate restriced carbohydrate diet formula (MCD, Treat group) in a specific pathogen free zone. All procedures were approved by the institutional animal use and care committee. Following a preliminary feeding of each diet formula for two week, HrasG12V / shp53 / GFP4 gene containing transposon vector were injected into mouse tail vein by hydrodynamic injection method. After 4 weeks of diet supplementation, all mice were sacrificed. Mouse liver tissue was excised for microarray analysis.
2012-05-04 | E-GEOD-37762 | biostudies-arrayexpress