ArticleRedox biology2017
Polychlorinated biphenyls-153 induces metabolic dysfunction through activation of ROS/NF-κB signaling via downregulation of HNF1b.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Association between polychlorinated biphenyl (PCB) and dioxin with metabolic syndrome (METS): a systematic review and meta-analysis.Scientific reports · 2024Pooled it
- Elephant Seal Blubber Under Multiple Stressors: Persistent Organic Pollutants, Stress Hormones and Hydrostatic Pressure Alter Transcriptome, Lipolysis and Leptin Secretion.Environmental science & technology · 2026Article
- Review
- Systemic control of HNF1B-driven redox homeostasis by N6-adenosine methylation.Nucleic acids research · 2026Article
- Association of Persistent Organic Pollutants Polychlorinated Biphenyls and Dioxins with Cardiovascular-Kidney-Metabolic Syndrome and Its Prognosis: A Nationally Representative Study.Cardiorenal medicine · 2026Article
- Hepatocyte nuclear factor 1 in renal lipid metabolism: molecular mechanisms and therapeutic potentials.Cell biology and toxicology · 2025Review
- Mixtures ofToxics · 2025Article
- Hepatocyte nuclear factors dynamically regulate triglyceride metabolic reprogramming in metabolic dysfunction-associated steatotic liver disease: Mechanisms and implications.World journal of hepatology · 2025Review
- Serum copper modulates cognitive function in diabetic patients via an HDL-C-mediated pathway: identification of a 25 µg/dL exploratory threshold.Diabetology & metabolic syndrome · 2025Article
- Review
- Chimeric exosomes-derived immunomodulator restoring lymph nodes microenvironment for sensitizing TNBC immunotherapy.Nature communications · 2025Article
- The relationship between metabolic syndrome and environmental endocrine disruptors: A systematic review and meta-analysis.iScience · 2025Article
- miR-504-3p-HNF1B signaling axis aggravates podocyte injury in diabetic kidney disease.Journal of molecular histology · 2025Article
- Primitive to visceral endoderm maturation is essential for mouse epiblast survival beyond implantation.iScience · 2025Article
- Endocrine disruptors, insulin resistance, and diabetes.Turkish journal of medical sciences · 2025Review
- Upregulation of fatty acid synthesis genes in the livers of adolescent female rats caused by inhalation exposure to PCB52 (2,2',5,5'-Tetrachlorobiphenyl).Environmental toxicology and pharmacology · 2024Article
- Inflammation and cardiometabolic diseases induced by persistent organic pollutants and nutritional interventions: Effects of multi-organ interactions.Environmental pollution (Barking, Essex : 1987) · 2023Review
- Effects of Indoor Dust Exposure on Lung Cells: Association of Chemical Composition with Phenotypic and Lipid Changes in a 3D Lung Cancer Cell Model.Environmental science & technology · 2023Article
- Sortilin-induced lipid accumulation and atherogenesis are suppressed by HNF1b SUMOylation promoted by flavone ofJournal of Zhejiang University. Science. B · 2023Article
- Neuroprotective Effect of Hydrogen Sulfide Subchronic Treatment Against TBI-Induced Ferroptosis and Cognitive Deficits Mediated Through Wnt Signaling Pathway.Cellular and molecular neurobiology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polychlorinated biphenyls (PCB) is a major type of persistent organic pollutants (POPs) that act as endocrine-disrupting chemicals. In the current study, we examined the mechanism underlying the effect of PCB-153 on glucose and lipid metabolism in vivo and in vitro. We found that PCB-153 induced per se and worsened high fat diet (HFD)-resulted increase of blood glucose level and glucose and insulin intolerance. In addition, PCB-153 induced per se and worsened HFD-resulted increase of triglyceride content and adipose mass. Moreover, PCB-153 concentration-dependently inhibited insulin-dependent glucose uptake and lipid accumulation in cultured hepatocytes and adipocytes. PCB-153 induced the expression and nuclear translocation of p65 NF-κB and the expression of its downstream inflammatory markers, and worsened HFD-resulted increase of those inflammatory markers. Inhibition of NF-κB significantly suppressed PCB-153-induced inflammation, lipid accumulation and decrease of glucose uptake. PCB-153 induced oxidative stress and decreased hepatocyte nuclear factor 1b (HNF1b) and glutathione peroxidase 1 (GPx1) expression in vivo and in vitro. Overexpression of HNF1b increased GPx1 expression, decreased ROS level, decreased Srebp1, ACC and FAS expression, and inhibited PCB-153-resulted oxidative stress, NF-κB-mediated inflammation, and final glucose/lipid metabolic disorder. Our results suggest that dysregulation of HNF1b/ROS/NF-κB plays an important role in PCB-153-induced glucose/lipid metabolic disorder.
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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 OpenQuestion graph.