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Related Concept Videos

Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
Co-activators and Co-repressors02:04

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TGF - β Signaling Pathway01:16

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Cell Specific Gene Expression01:58

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Liver Regeneration01:24

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Related Experiment Video

Updated: Jul 17, 2026

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
09:44

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

Tumor necrosis factor and interleukin 1 decrease RXRalpha, PPARalpha, PPARgamma, LXRalpha, and the coactivators

Min Sun Kim1, Trevor R Sweeney, Judy K Shigenaga

  • 1Department of Medicine, University of California San Francisco, San Francisco, CA 94143, USA.

Metabolism: Clinical and Experimental
|January 17, 2007
PubMed
Summary

Cytokines like TNF and IL-1 reduce key nuclear receptors and coactivators involved in lipid metabolism, contributing to altered liver function during the acute phase response.

Related Experiment Videos

Last Updated: Jul 17, 2026

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
09:44

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

Area of Science:

  • Molecular Biology
  • Metabolic Regulation
  • Cellular Signaling

Background:

  • Cytokines orchestrate the acute phase response, significantly impacting lipid metabolism.
  • Previous studies noted changes in serum triglycerides, fatty acid oxidation, bile acid synthesis, and HDL levels during this response.

Purpose of the Study:

  • To investigate the effect of specific cytokines, tumor necrosis factor (TNF) and interleukin 1 (IL-1), on the expression of nuclear hormone receptors and coactivators in hepatic cells.
  • To elucidate the molecular mechanisms underlying cytokine-induced alterations in hepatic lipid metabolism.

Main Methods:

  • Treatment of Hep3B human hepatoma cells and mice with TNF and IL-1.
  • Quantitative analysis of messenger RNA (mRNA) levels for retinoid X receptor alpha (RXRalpha), peroxisome proliferator-activated receptors (PPARalpha, PPARgamma), liver X receptor alpha (LXRalpha), and coactivators (PGC-1alpha, PGC-1beta, SRC-1).
  • Assessment of nuclear extract binding to response elements and luciferase reporter assays.
  • Measurement of mRNA levels for downstream target genes regulated by PPARalpha and LXR.
  • Analysis of promoter activity using luciferase constructs.

Main Results:

  • TNF and IL-1 significantly decreased the expression of RXRalpha, PPARalpha, PPARgamma, LXRalpha, PGC-1alpha, PGC-1beta, and SRC-1 in Hep3B cells and mouse liver.
  • These reductions were associated with decreased DNA binding activity and transcriptional activity of PPAR and LXR.
  • mRNA levels of key metabolic enzymes regulated by PPARalpha and LXR were also diminished.
  • Decreased transcription of LXRalpha and PGC-1alpha promoters was observed, indicating transcriptional downregulation.

Conclusions:

  • The study demonstrates that TNF and IL-1 suppress the expression of critical nuclear hormone receptors and coactivators in the liver.
  • This suppression, driven by decreased transcription, likely contributes to the altered hepatic lipid metabolism observed during the acute phase response.
  • Targeting these pathways could offer therapeutic strategies for managing metabolic dysregulation during inflammation.