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Updated: Jun 27, 2026

Real-time Analyses of Retinol Transport by the Membrane Receptor of Plasma Retinol Binding Protein
14:32

Real-time Analyses of Retinol Transport by the Membrane Receptor of Plasma Retinol Binding Protein

Published on: January 28, 2013

Fenofibrate reduces serum retinol-binding protein-4 by suppressing its expression in adipose tissue

Haiya Wu1, Li Wei, Yuqian Bao

  • 1Department of Endocrinology and Metabolism, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, 600 Yishan Rd., Shanghai 200233, China.

American Journal of Physiology. Endocrinology and Metabolism
|December 18, 2008
PubMed

Insights

Fenofibrate treatment lowers serum retinol-binding protein-4 (RBP4) levels in patients with dyslipidemia. This reduction in RBP4, an adipocytokine linked to insulin resistance, may explain how fenofibrate improves insulin sensitivity.

Area of Science:

  • Metabolic Research
  • Endocrinology
  • Pharmacology

Background:

  • Fenofibrate is a peroxisome proliferator-activated receptor-alpha (PPARalpha) activator used for dyslipidemia and insulin resistance.
  • Retinol-binding protein-4 (RBP4) is an adipocytokine implicated in linking obesity with insulin resistance.
  • The molecular mechanisms of fenofibrate's action, particularly concerning RBP4, require further elucidation.

Purpose of the Study:

  • To investigate the effect of fenofibrate on serum retinol-binding protein-4 (RBP4) levels in dyslipidemic patients.
  • To explore the biochemical mechanisms by which fenofibrate influences RBP4 expression.
  • To determine if fenofibrate's inhibition of RBP4 contributes to improved insulin sensitivity.

Main Methods:

  • Clinical study involving dyslipidemic patients treated with fenofibrate.
  • Animal study using obese rats to assess fenofibrate's effect on RBP4 mRNA in adipose tissue and liver.
  • In vitro study using 3T3-L1 adipocytes to examine fenofibrate's direct impact on RBP4 expression.

Main Results:

  • Fenofibrate treatment significantly decreased serum RBP4 levels in dyslipidemic patients, correlating with reduced body weight and enhanced insulin sensitivity.
  • In obese rats, fenofibrate markedly reduced RBP4 mRNA levels in adipose tissue but not the liver, correlating with decreased serum RBP4 and improved insulin sensitivity.
  • Fenofibrate treatment significantly reduced RBP4 mRNA expression in 3T3-L1 adipocytes, indicating a direct effect on adipocytes.

Conclusions:

  • Fenofibrate inhibits RBP4 expression in dyslipidemic human subjects.
  • The inhibition of RBP4 expression in adipocytes by fenofibrate may be a key mechanism for improving insulin sensitivity.
  • These findings provide novel insights into the molecular pathways through which fenofibrate exerts its therapeutic effects.

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