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E-MEXP-490

ABSTRACT: Transcription profiling by array of liver from db/db mice after treatment with metformin

PROVIDER: E-MEXP-490 | ExpressionAtlas | 2014-07-03

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MEXP-490-analysis-methods.tsv	Tabular
	E-MEXP-490-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-490-configuration.xml	Xml
	E-MEXP-490-percentile-ranks.tsv	Tabular
	E-MEXP-490.condensed-sdrf.tsv	Tabular

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Pleiotropic effects of metformin on inflammation, oxidative and dicarbonyl stress in transgenic spontaneously hypertensive rats expressing human C-reactive protein.

Project description:Inflammation, oxidative and dicarbonyl stress play important roles in the pathophysiology of type 2 diabetes. Metformin is the first-line drug of choice for the treatment of type 2 diabetes because it effectively suppresses gluconeogenesis in the liver, however, its “pleiotropic“ effects remain controversial. In the current study, we tested the effects of metformin on inflammation, oxidative and dicarbonyl stress in an animal model of inflammation and metabolic syndrome, the spontaneously hypertensive rat transgenically expressing human C-reactive protein (SHR-CRP). In the SHR-CRP transgenic strain, we found that metformin treatment decreased circulating levels of inflammatory response marker IL6 while levels of human CRP remained unchanged and metformin also significantly reduced oxidative stress (levels of conjugated dienes and TBARS) in the liver while no significant effects were observed in SHR control rats. In addition, in the presence of high human CRP, metformin reduced methylglyoxal levels in left ventricles but not in kidneys. Finally, metformin treatment reduced adipose tissue lipolysis. Possible molecular mechanisms of metformin action studied by gene expression profiling in the liver revealed deregulated genes from inflammatory, insulin signaling, AMP-activated protein kinase (AMPK) signaling and gluconeogenesis pathways. It can be concluded that in the presence of high levels of human CRP metformin protects against inflammation, oxidative and dicarbonyl stress in the heart and ameliorates insulin resistance and dyslipidemia.

2016-07-03 | E-MTAB-3791 | biostudies-arrayexpress

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Project description:Mouse liver transcription profiling by array

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Transcriptomic profiling across 20 CC-RIX genetic backgrounds with and without high-fat high-sugar (HFHS) diet, and with and without metformin [skeletal muscle]

Project description:Adipose, liver, and skeletal muscle tissue from 6-month and 12-month CC-RIX cohorts underwent transcriptomic profiling. CC-RIX cohorts were exposed to sensitizer (HFHS diet) and a widely used pharmaceutical intervention (metformin). Chow (control) or high fat high sugar (HFHS) diet started at 6 weeks of age.. At six months of age, a subset of mice from each chow group and of each sex were euthanized for tissue collection. At 7 months of age, half of the remaining mice in each diet treatment group will receive metformin treatment. In a subset of the 12 month cohort animals, metformin (5 mg/mL) was delivered ad libitum in the drinking water (Chang, Moro et al. 2018). Terminal phenotyping and tissue collection was done at 12 months of age.

2024-11-05 | GSE237747 | GEO

Transcriptomic profiling across 20 CC-RIX genetic backgrounds with and without high-fat high-sugar (HFHS) diet, and with and without metformin [liver]

2024-11-05 | GSE237743 | GEO

Transcriptomic profiling across 20 CC-RIX genetic backgrounds with and without high-fat high-sugar (HFHS) diet, and with and without metformin [adipose]

2024-11-05 | GSE237737 | GEO

Expression data from mouse liver treated with metformin

Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.

2012-02-21 | E-GEOD-35961 | biostudies-arrayexpress

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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Mus musculus

Project description:Transcription profiling of mouse liver by array

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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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Quantitative In Vivo Proteomics of Metformin Response in Liver Reveals AMPK-Dependent and -Independent Signaling Networks

Project description:Metformin is the front-line treatment for type 2 diabetes worldwide. It acts via effects on glucose and lipid metabolism in metabolic tissues, leading to enhanced insulin sensitivity. Despite significant effort, the molecular basis for metformin response remains poorly understood, with a limited number of specific biochemical pathways studied to date. To broaden our understanding of hepatic metformin response, we combine phospho-protein enrichment in tissue from genetically engineered mice with a quantitative proteomics platform to enable the discovery and quantification of basophilic kinase substrates in-vivo. We define proteins that binding to 14-3-3 are acutely regulated by metformin treatment and/or loss of the serine/threonine kinase, LKB1. Inducible binding of 250 proteins following metformin treatment is observed, 44% LKB1-dependent. Beyond AMPK, metformin activates Protein Kinase D and MAPKAPK2 in an LKB1-independent manner, revealing additional kinases that may mediate aspects of metformin response. Deeper analysis uncovered substrates of AMPK in endocytosis and calcium homeostasis.

2019-10-07 | MSV000084429 | MassIVE

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