Related Experiment Videos
Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules
Haiyan Song1, Nobuhiro Shojima, Hideyuki Sakoda
1Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, 113, Tokyo, Japan.
Biochemical and Biophysical Research Communications
|November 20, 2002
Summary
Resistin expression, linked to insulin resistance, is controlled by transcription factors C/EBPalpha and PPARgamma. Signaling pathways like PI3-kinase and MAP kinase also regulate resistin levels.
Area of Science:
- Molecular Biology
- Endocrinology
- Cell Biology
Background:
- Resistin, an adipocyte-derived protein, is implicated in insulin resistance.
- Its expression is modulated by hormones like insulin and TNFalpha.
- Understanding resistin regulation is crucial for metabolic research.
Purpose of the Study:
- To identify transcription factors and signaling pathways influencing resistin expression in 3T3-L1 adipocytes.
- To elucidate the molecular mechanisms controlling resistin gene expression.
Main Methods:
- Adenovirus-mediated gene transfer was employed in 3T3-L1 adipocytes.
- Overexpression of specific transcription factors (C/EBPalpha, C/EBPzeta, PPARgamma, PPARalpha) and signaling molecules (PI3-kinase, Akt, MEK1, MKK6, MKK7) was performed.
Main Results:
- C/EBPalpha enhanced resistin expression, while C/EBPzeta suppressed it.
- PPARgamma significantly reduced resistin expression; PPARalpha had no effect.
- PI3-kinase, Akt, MEK1, MKK6, and MKK7 overexpression suppressed resistin expression.
Conclusions:
- Resistin expression is regulated by C/EBPalpha and PPARgamma.
- These factors modulate resistin partly through the PI3-kinase and MAP kinase signaling pathways.
- Findings provide insights into the molecular control of resistin in adipocytes.