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Contribution of glucocorticoid-mineralocorticoid receptor pathway on the obesity-related adipocyte dysfunction

Ayumu Hirata1, Norikazu Maeda, Hideaki Nakatsuji

  • 1Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, 2-2-B5 Yamada-oka, Suita, Osaka 565-0871, Japan. hirata@endmet.med.osaka-u.ac.jp

Biochemical and Biophysical Research Communications
|February 14, 2012
PubMed
Abstract

Insights

Mineralocorticoid receptor (MR) blockade improves obesity-related issues by targeting glucocorticoids. This pathway may explain adipocytokine dysregulation and reactive oxygen species (ROS) in adipose tissue.

Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Obesity Research

Background:

  • Mineralocorticoid receptor (MR) blockade shows promise in improving insulin resistance, adipocytokine dysregulation, inflammation, and reactive oxygen species (ROS) in obesity.
  • The precise mechanism by which MR blockade exerts these effects, particularly concerning the role of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and glucocorticoid action, remains unclear.

Purpose of the Study:

  • To investigate if glucocorticoids influence adipocytokines and ROS via MR in adipocytes.
  • To examine the distribution of MR and glucocorticoid receptor (GR) in human adipose tissue.

Main Methods:

  • Analysis of corticoid receptors and target genes in obese db/db mice adipose tissue.
  • Treatment of 3T3-L1 adipocytes with glucocorticoids, H2O2, MR antagonist eplerenone (EP), GR antagonist RU486 (RU), MR-siRNA, and N-acetylcysteine.
  • Investigation of MR and GR mRNA levels in human adipose tissue from patients undergoing abdominal surgery.

Main Results:

  • Obese mice exhibited higher mRNA levels of MR and its target genes compared to controls.
  • Glucocorticoids induced adipocytokine gene dysregulation and increased intracellular ROS in adipocytes, effects reversed by MR blockade but not GR antagonism.
  • Human visceral fat showed increased MR mRNA levels correlated with BMI, unlike GR mRNA levels.

Conclusions:

  • The glucocorticoid-MR pathway is implicated in obesity-related adipocytokine dysregulation and adipose tissue ROS.
  • MR blockade represents a potential therapeutic strategy for managing obesity-associated metabolic disturbances.

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