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beta-adrenoceptor agonists downregulate adiponectin, but upregulate adiponectin receptor 2 and tumor necrosis

Ling Fu1, Kazumasa Isobe, Qin Zeng

  • 1Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.

European Journal of Pharmacology
|June 19, 2007
PubMed

Insights

Beta-adrenoceptor activation downregulates adiponectin and upregulates TNF-alpha, potentially contributing to insulin resistance. Upregulation of adiponectin receptor 2 may be a feedback response to reduced adiponectin levels.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Adipose Tissue Biology

Background:

  • Adiponectin enhances insulin sensitivity, while TNF-alpha promotes insulin resistance.
  • Previous studies suggest mutual inhibition of adiponectin and TNF-alpha production in adipocytes.
  • Beta(3)-adrenoceptor agonists are investigated for their metabolic effects.

Purpose of the Study:

  • To investigate the effects of beta(3)-adrenoceptor agonists (CL-316,243 and BRL37344) on adiponectin, TNF-alpha, and their receptor gene expression in mouse adipose tissues.
  • To explore the impact of beta-adrenoceptor activation on adiponectin and TNF-alpha in 3T3-L1 adipocytes.

Main Methods:

  • Administration of beta(3)-adrenoceptor agonists CL-316,243 and BRL37344 to C57BL/6J mice.
  • Gene expression analysis of adiponectin, adiponectin receptors (1 and 2), and TNF-alpha in various adipose tissues.
  • Treatment of differentiated 3T3-L1 adipocytes with isoproterenol (a non-selective beta-adrenoceptor agonist).
  • Measurement of TNF-alpha protein expression and adiponectin secretion in treated adipocytes.

Main Results:

  • CL-316,243 and BRL37344 downregulated adiponectin and upregulated adiponectin receptor 2 (not receptor 1) in white and brown adipose tissues.
  • TNF-alpha expression was upregulated in epididymal adipose tissue following agonist treatment.
  • In 3T3-L1 adipocytes, isoproterenol decreased adiponectin expression/secretion but increased adiponectin receptor 2 and TNF-alpha protein expression.
  • Signaling pathways involving adenylyl cyclase, PKA, and AMPK were implicated in the observed effects.

Conclusions:

  • Beta-adrenoceptor activation leads to decreased adiponectin and increased TNF-alpha, potentially contributing to catecholamine-induced insulin resistance.
  • Upregulation of adiponectin receptor 2 appears to be a compensatory response to reduced adiponectin levels.
  • These findings highlight a complex interplay between beta-adrenergic signaling, adipokines, and insulin resistance.

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