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E-GEOD-35961

ABSTRACT: Expression data from mouse liver treated with metformin

OTHER RELATED OMICS DATASETS IN: PRJNA152055

PROVIDER: E-GEOD-35961 | ExpressionAtlas | 2015-09-28

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-35961-analysis-methods.tsv	Tabular
	E-GEOD-35961-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-35961-configuration.xml	Xml
	E-GEOD-35961-percentile-ranks.tsv	Tabular
	E-GEOD-35961.condensed-sdrf.tsv	Tabular

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Project description:Expression data from mouse liver treated with metformin

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Metabolomics Workbench ST000340 - GNPS - Metformin effects on liver and kidney tissue

Project description:This experiment aimed to discover the effects of metformin on mouse liver and kidney tissue. The effects were seen by comparing the liver of the metformin group to the liver of a control group of mice treated given saline solution.

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Study of microRNA associated with metformin treatment in a mouse model of NASH(MCD)

Project description:The microRNAs expression was altered with the treatment of metformin in vivo and several microRNAs induced by metformin also may contribute to suppressed of NASH. Using a custom microarray platform, we analyzed the expression levels of 1135 mouse microRNA probes in liver tissue in vivo that were treated with and without metformin.

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Transcriptome profiling of wildtype C57BL/6 mouse with metformin treatment

Project description:Background: Metformin, one of the first-line medication for the treatment of type 2 diabetes and gestational diabetes, has recently be suggested for targeting cardiovascular disease, cancer and aging. Therefore, current understanding of the mechanism of this drug is incompletely understood, and the function of multiple tissues, other than liver metabolism alone, may be influenced. Methods: The wildtype healthy mice treated with metformin were compared with controls (treated with double distilled water). The transcriptome changes with/without metformin treatment were probed by using high-throughput RNA-seq techniques Results: A comprehensive mouse transcriptome map with metformin treatment across ten tissues including aorta, eyeball, brain, adipose tissue, heart, kidney, liver, skeletal muscle, stomach and testis, was provided. Function enrichment, network characteristics and disease association of the differentially expressed genes were analyzed. We also compared our expression profiles with related microarray data in order to find conditions that share similar expression profiles with metformin treatment. Conclusions: This dataset could serve as a baseline resource for investigating the potential beneficial or adverse effects of metformin across different tissues.

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Genes Expression Analysis of Cervical Cancer-derived cells Treated with Metformin

Project description:NOD-SCID mouse were treated with metformin for 11 and 24 days, the gene expression of tumors of mice treated with metformin were compared with respect to the expression of the tumors of mouse treated with vehicle (water). We evaluated the effect of Metformin (525mg/kg/day) for two times of treatment (11 days and 24 days) upon gene expression in tumors of mice treated or not with metformin. Metformin treatment decreased of tumor growth in both treatment regimens. A complete genomic analysis of transcriptomic status after treatment with metformin revealed an impact on the overall expression of transcripts.

2025-01-31 | GSE144395 | GEO

Gene expression analysis of micoRNA-221 overexpressing transgenic mice livers with and without metformin intervention upon chronic liver injury induced by carbon tetrachloride

Project description:Metformin is a hypoglycaemic agent used to treat type 2 diabetes mellitus (DM2) patients, with a broad safety profile. Since previous epidemiological studies had shown that incidence of hepatocellular carcinoma (HCC) decreased significantly in metformin treated DM2 patients, we hypothesized that intervention with metformin could reduce the risk of neoplastic transformation of hepatocytes. HCC is the most common primary liver malignancy and it generally originates in a background of liver fibrosis and cirrhosis. In the present study, we took advantage of a transgenic mouse (TG221) characterized by microRNA-221 overexpression, with cirrhotic liver background induced by chronic administration of carbon tetrachloride (CCl4). This mouse model develops fibrosis, cirrhosis and liver tumors that become visible in 100% of mice at 5-6 months of age.

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Metformin Induces Dicer via Regulation of the RNA-binding protein AUF1

Project description:Metformin has been commonly used for decades to treat type 2 diabetes. Recent data indicates that mice treated with metformin live longer and healthier lives. Here, we show that chronic metformin exposure in mice and diabetics taking metformin have higher levels of the microRNA processing protein, Dicer. Examination of how metformin affects Dicer expression revealed that metformin alters binding of the AUF1 RNA-binding protein to DICER1 mRNA, which leads to stabilization of DICER1 mRNA. We found differential changes in microRNA expression in mice treated with metformin or caloric restriction, a proven life extending intervention. Several of these microRNAs are important for regulating cellular senescence and lifespan in model organisms. Consistent with this observation, treatment with metformin decreased cellular senescence in a Dicer-dependent manner. These data lead us to hypothesize that changes in Dicer levels may be important for organismal aging and that interventions that upregulate Dicer expression (e.g., metformin) may offer new therapeutic approaches to combat or prevent age-related diseases. Key words: diabetes mellitus, metformin, senescence, miRNA, RNA-binding proteins

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Importance of AMPK in metformin suppression of liver glucose production

Project description:Metformin is now the most widely prescribed oral anti-diabetic agent worldwide, taken by over 150 million people annually. Although metformin has been used clinically to treat type 2 diabetes for over 60 years. Its mechanism of action remains only partially understood and controversial. In particular, this includes whether AMPK plays a role in metformin suppression of liver glucose production. To address this issue, we knocked out the AMPK catalytic alpha1 and alpha 2 subunits in the liver of HFD-fed adult homozygous mice. These mice were treated with a physiological relevent metformin dose (50 mg/kg/day) for 3 weeks. Liver samples were collected.

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Primary Mouse Hepatocytes treated with 500μM Metformin for 24 hours

Project description:Anaylsis of gene expression in primary mouse hepatocytes treated with 500μM Metformin for 24 hours

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