ArticleToxicological sciences : an official journal of the Society of Toxicology2018
PCB126 Inhibits the Activation of AMPK-CREB Signal Transduction Required for Energy Sensing in Liver.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Single-cell transcriptomics showed that maternal polychlorinated biphenyl exposure dysregulated cell type-specific metabolic responses in the livers of female mouse offsprings.Drug metabolism and disposition: the biological fate of chemicals · 2026Article
- Sex-dependent modulation of PCB-mediated toxicity from a proteomic and microbiome perspective.Scientific reports · 2025Article
- Complex roles for sulfation in the toxicities of polychlorinated biphenyls.Critical reviews in toxicology · 2024Review
- Transcriptome sequencing of 3,3',4,4',5-Pentachlorobiphenyl (PCB126)-treated human preadipocytes demonstrates progressive changes in pathways associated with inflammation and diabetes.Toxicology in vitro : an international journal published in association with BIBRA · 2022Article
- CYP1A1, VEGFA and Adipokine Responses of Human Adipocytes Co-exposed to PCB126 and Hypoxia.Cells · 2022Article
- PCB126 induced toxic actions on liver energy metabolism is mediated by AhR in rats.Toxicology · 2022Article
- Proteomics and metabolic phenotyping define principal roles for the aryl hydrocarbon receptor in mouse liver.Acta pharmaceutica Sinica. B · 2021Article
- The Aryl hydrocarbon receptor mediates reproductive toxicity of polychlorinated biphenyl congener 126 in rats.Toxicology and applied pharmacology · 2021Article
- Skeletal toxicity resulting from exposure of growing male rats to coplanar PCB 126 is associated with disruption of calcium homeostasis and the GH-IGF-1 axis and direct effects on bone formation.Archives of toxicology · 2020Article
- Understanding the Multiple Effects of PCBs on Lipid Metabolism.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- Exposure to Persistent Organic Pollutants (POPs) and Their Relationship to Hepatic Fat and Insulin Insensitivity among Asian Indian Immigrants in the United States.Environmental science & technology · 2019Article
- Mechanisms of Environmental Contributions to Fatty Liver Disease.Current environmental health reports · 2019Review
- Identifying sex differences arising from polychlorinated biphenyl exposures in toxicant-associated liver disease.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2019Article
- Polychlorinated Biphenyls and Nonalcoholic Fatty Liver Disease.Current opinion in toxicology · 2019Article
- Hepatic signalling disruption by pollutant Polychlorinated biphenyls in steatohepatitis.Cellular signalling · 2019Article
- Polychlorinated biphenyl 126 exposure in rats alters skeletal muscle mitochondrial function.Environmental science and pollution research international · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
3,3',4,4',5-pentachlorobiphenyl (PCB126), a dioxin-like PCB, elicits toxicity through a wide array of noncarcinogenic effects, including metabolic syndrome, wasting, and nonalcoholic fatty-liver disease. Previously, we reported decreases in the transcription of several enzymes involved in gluconeogenesis, before the early onset of lipid accumulation. Hence, this study was aimed at understanding the impact of resultant decreases gluconeogenic enzymes on growth, weight, and metabolism in the liver, upon extended exposure. Male Sprague Dawley rats (75-100 g), fed a defined AIN-93G diet, were injected (ip) with single dose of soy oil (5 ml/kg body weight; n = 14) or PCB126 (5 µmol/kg; n = 15), 28 days, prior euthanasia. A subset of rats from each group were fasted for 12 h (vehicle [n = 6] and PCB126 [n = 4]). Rats only showed significant weight loss between days 14 and 28 (p < .05) and some mortality (p = .0413). As in our previous studies, the expression levels of enzymes involved in gluconeogenesis (Pepck-c, G6Pase, Sds, Pc, and Ldh-A) and glycogenolysis (Pygl) were strongly downregulated. The decreased expression of these enzymes in PCB126-treated rats after a 12 h fast decreased hepatic glucose production from glycogen and gluconeogenic substrates, exacerbating the hypoglycemia. Additionally, PCB126 caused hepatic steatosis and decreased the expression of the transcription factor Pparα and its targets, necessary for fatty-acid oxidation. The observed metabolic disruption across multiple branches of fasting metabolism resulted from inhibition in the activation of enzyme AMPK and transcription factor CREB signaling, necessary for "sensing" energy-deprivation and the induction of enzymes that respond to the PCB126 triggered fuel crisis in liver.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.