ArticleGene expression2009
Conditional ablation of mediator subunit MED1 (MED1/PPARBP) gene in mouse liver attenuates glucocorticoid receptor agonist dexamethasone-induced hepatic steatosis.
Article in Gene expression, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- Hepatic Glucocorticoid Receptor Action and Glucose Homeostasis.Endocrine reviews · 2026Review
- Modulating glucocorticoid receptor actions in physiology and pathology: Insights from coregulators.Pharmacology & therapeutics · 2023Review
- Steroid-mediated liver steatosis is CD1d-dependent, while steroid-induced liver necrosis, inflammation, and metabolic changes are CD1d-independent.BMC gastroenterology · 2022Article
- Detailed Molecular Mechanisms Involved in Drug-Induced Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: An Update.Biomedicines · 2022Review
- Molecular Mechanisms of Glucocorticoid-Induced Insulin Resistance.International journal of molecular sciences · 2021Review
- E47 modulates hepatic glucocorticoid action.Nature communications · 2019Article
- Mediator 1 Is Atherosclerosis Protective by Regulating Macrophage Polarization.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Establishment of a mouse model of enalapril-induced liver injury and investigation of the pathogenesis.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Cardiac Med1 deletion promotes early lethality, cardiac remodeling, and transcriptional reprogramming.American journal of physiology. Heart and circulatory physiology · 2017Article
- Regulation of metabolism by the Mediator complex.Biophysics reports · 2016Article
- Minireview: new molecular mediators of glucocorticoid receptor activity in metabolic tissues.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Med1 subunit of the mediator complex in nuclear receptor-regulated energy metabolism, liver regeneration, and hepatocarcinogenesis.Gene expression · 2014Review
- The Med1 subunit of the mediator complex induces liver cell proliferation and is phosphorylated by AMP kinase.The Journal of biological chemistry · 2013Article
- Dexamethasone reduces energy expenditure and increases susceptibility to diet-induced obesity in mice.Obesity (Silver Spring, Md.) · 2013Article
- The Mediator Complex and Lipid Metabolism.Journal of biochemical and pharmacological research · 2013Article
- Regulation of triglyceride metabolism by glucocorticoid receptor.Cell & bioscience · 2012Article
- Secondary causes of nonalcoholic fatty liver disease.Therapeutic advances in gastroenterology · 2012Article
- Mediator-dependent nuclear receptor function.Seminars in cell & developmental biology · 2011Review
- PPARalpha: energy combustion, hypolipidemia, inflammation and cancer.Nuclear receptor signaling · 2010Review
- Transcription coactivator PBP/MED1-deficient hepatocytes are not susceptible to diethylnitrosamine-induced hepatocarcinogenesis in the mouse.Carcinogenesis · 2010Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Glucocorticoid receptor (GR) agonist dexamethasone (Dex) induces hepatic steatosis and enhances constitutive androstane receptor (CAR) expression in the liver. CAR is known to worsen hepatic injury in nonalcoholic hepatic steatosis. Because transcription coactivator MED1/PPARBP gene is required for GR- and CAR-mediated transcriptional activation, we hypothesized that disruption of MED1/PPARBP gene in liver cells would result in the attenuation of Dex-induced hepatic steatosis. Here we show that liver-specific disruption of MED1 gene (MED1(delta Liv)) improves Dex-induced steatotic phenotype in the liver. In wild-type mice Dex induced severe hepatic steatosis and caused reduction in medium- and short-chain acyl-CoA dehydrogenases that are responsible for mitochondrial beta-oxidation. In contrast, Dex did not induce hepatic steatosis in mice conditionally null for hepatic MED1, as it failed to inhibit fatty acid oxidation enzymes in the liver. MED1(delta Liv) livers had lower levels of GR-regulated CAR mRNA compared to wild-type mouse livers. Microarray gene expression profiling showed that absence of MED1 affects the expression of the GR-regulated genes responsible for energy metabolism in the liver. These results establish that absence of MED1 in the liver diminishes Dex-induced hepatic steatosis by altering the GR- and CAR-dependent gene functions.
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