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Related Experiment Video

Updated: Jul 3, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Regulation of PPARgamma function by TNF-alpha.

¹Pennington Biomedical Research Center, Louisiana State University System, 6400 Perkins Road, Baton Rouge, LA 70808, USA. yej@pbrc.edu

Biochemical and Biophysical Research Communications

|July 29, 2008

Summary

Tumor necrosis factor-alpha (TNF-alpha) inhibits the lipid-regulating nuclear receptor PPARgamma, impacting metabolic diseases. This review details how TNF-alpha, particularly via IKK signaling, disrupts PPARgamma activity at multiple levels.

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Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells

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Last Updated: Jul 3, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

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Published on: June 3, 2016

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells

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Published on: March 28, 2013

Area of Science:

Molecular Biology
Metabolic Regulation
Cell Signaling

Background:

Peroxisome proliferator-activated receptor gamma (PPARgamma) is a key nuclear receptor regulating lipid metabolism and gene transcription.
PPARgamma dysfunction is implicated in metabolic disorders like insulin resistance, atherosclerosis, inflammation, and cancer cachexia.
Tumor necrosis factor-alpha (TNF-alpha) is a critical mediator that inhibits PPARgamma activity.

Purpose of the Study:

To review the molecular mechanisms by which TNF-alpha inhibits PPARgamma activity.
To elucidate the role of serine kinases, particularly IKK, in TNF-alpha-mediated PPARgamma regulation.
To provide a comprehensive overview of pre-translational and post-translational regulation of PPARgamma by TNF-alpha.

Main Methods:

Literature review focusing on studies investigating PPARgamma regulation by TNF-alpha.
Analysis of signaling pathways involving serine kinases (IKK, ERK, JNK, p38) in TNF-alpha's effects on PPARgamma.
Examination of mechanisms including gene expression inhibition and corepressor activation.

Main Results:

TNF-alpha inhibits PPARgamma activity through both pre-translational and post-translational modifications.
Activation of serine kinases, with IKK being a dominant player, is central to TNF-alpha's inhibitory effects.
IKK mediates inhibition via suppressing PPARgamma expression and activating its corepressor.

Conclusions:

TNF-alpha significantly impairs PPARgamma function, contributing to various pathologies.
The IKK signaling pathway is a primary mediator of TNF-alpha's inhibitory actions on PPARgamma.
Understanding these mechanisms is crucial for developing therapeutic strategies targeting metabolic diseases.