Multi-omics analysis reveals BPF exposure causes hepatic glucose and lipid metabolism disorder in rats by disrupting energy homeostasis
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View abstract on PubMed
Summary
This summary is machine-generated.Bisphenol F (BPF) exposure damages the liver and disrupts glucose and lipid metabolism in rats. BPF alters key metabolic pathways, impacting fatty acid and glucose regulation.
Area Of Science
- Toxicology
- Metabolic Disorders
- Environmental Health
Background
- Bisphenol F (BPF) is a common substitute for Bisphenol A (BPA) in consumer products.
- BPF poses risks to human health via environmental and food chain contamination.
- The specific effects of BPF on liver toxicity and metabolism are not well understood.
Purpose Of The Study
- To investigate the hepatotoxicity of BPF in a rat model.
- To determine the impact of BPF on glucose and lipid metabolism.
- To elucidate the molecular mechanisms underlying BPF-induced metabolic disruption.
Main Methods
- Male Sprague-Dawley rats were exposed to BPF.
- Histopathological examination (HE staining) and biochemical analyses of liver and serum were performed.
- Metabolomics and proteomics analyses were conducted on liver tissues.
- Gene and protein expression related to glucose and lipid metabolism were validated.
Main Results
- BPF exposure caused liver structural damage and dysfunction.
- Significant alterations in glucose and lipid metabolism were observed.
- BPF modulated fatty acid oxidation/synthesis via AMPK and PPAR pathways.
- BPF promoted glycogen synthesis and gluconeogenesis through the AKT pathway.
Conclusions
- BPF exhibits significant hepatotoxicity and disrupts liver glucose and lipid metabolism.
- Molecular pathways including AMPK, PPAR, and AKT are implicated in BPF's metabolic effects.
- These findings highlight the potential health risks associated with BPF exposure.
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