ArticleChemico-biological interactions2019
Hepatic metabolic adaptation in a murine model of glutathione deficiency.
Article in Chemico-biological interactions, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Trial
- Transcriptomic and Proteomic Insights into 6PPD/6PPD-Q Induced Oxidative Stress in Black-Spotted Frogs.Antioxidants (Basel, Switzerland) · 2025Article
- Liver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency.Chemico-biological interactions · 2024Article
- Glutathione synthesis in the mouse liver supports lipid abundance through NRF2 repression.Nature communications · 2024Article
- Persistence of improved glucose homeostasis in Gclm null mice with age and cadmium treatment.Redox biology · 2022Article
- Untargeted metabolomics as a diagnostic tool in NAFLD: discrimination of steatosis, steatohepatitis and cirrhosis.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- Age differences in brain structural and metabolic responses to binge ethanol exposure in fisher 344 rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Glutathione (GSH), the most abundant cellular non-protein thiol, plays a pivotal role in hepatic defense mechanisms against oxidative damage. Despite a strong association between disrupted GSH homeostasis and liver diseases of various etiologies, it was shown that GSH-deficient glutamate-cysteine ligase modifier subunit (Gclm)-null mice are protected against fatty liver development induced by a variety of dietary and environmental insults. The biochemical mechanisms underpinning this protective phenotype have not been clearly defined. The purpose of the current study was to characterize the intrinsic metabolic signature in the livers from GSH deficient Gclm-null mice. Global profiling of hepatic polar metabolites revealed a spectrum of changes in amino acids and metabolites derived from fatty acids, glucose and nucleic acids due to the loss of GCLM. Overall, the observed low GSH-driven metabolic changes represent metabolic adaptations, including elevations in glutamate, aspartate, acetyl-CoA and gluconate, which are beneficial for the maintenance of cellular redox and metabolic homeostasis.
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Registered trials
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