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Changes in adiponectin receptor expression in muscle and adipose tissue of type 2 diabetic patients during

G D Tan1, C Debard, T Funahashi

  • 1Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford OX3 7LJ, UK. garry.tan@oxlip.ox.ac.uk

Diabetologia
|July 2, 2005
PubMed
Abstract

Insights

Rosiglitazone alters adiponectin receptor 1 (adipoR1) expression differently in adipose tissue and skeletal muscle. This suggests adipoR1 plays a key role in mediating adiponectin

Area of Science:

  • Endocrinology and Metabolism
  • Molecular Biology
  • Pharmacology

Background:

  • Adiponectin is crucial for regulating insulin sensitivity in humans.
  • Adiponectin receptors (adipoR1 and adipoR2) have been identified but their tissue-specific expression and regulation by insulin-sensitizing agents remain unclear.

Purpose of the Study:

  • To investigate the regulation of adiponectin receptors (adipoR1/R2) and adiponectin expression in adipose tissue and skeletal muscle.
  • To assess changes in plasma adiponectin concentrations in response to rosiglitazone-induced insulin sensitization in patients with type 2 diabetes.

Main Methods:

  • A double-blind, placebo-controlled crossover study involving patients with type 2 diabetes.
  • Utilized in vivo arteriovenous techniques to measure adipose tissue and muscle blood flow.
  • Quantified adipose tissue and skeletal muscle gene expression and plasma adiponectin levels.

Main Results:

  • Rosiglitazone significantly increased plasma adiponectin concentrations by 69%.
  • AdipoR1 expression was upregulated in adipose tissue (p=0.02) but downregulated in skeletal muscle (p=0.04).
  • Adipose tissue adipoR1 upregulation correlated with improved triglyceride clearance and fatty acid output.

Conclusions:

  • AdipoR1 exhibits differential regulation in adipose tissue and skeletal muscle following insulin sensitization with rosiglitazone.
  • These findings indicate a tissue-specific role for adipoR1 in mediating the metabolic effects of adiponectin, particularly in relation to insulin sensitization.

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