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Cannabinoid type 1 receptor blockade promotes mitochondrial biogenesis through endothelial nitric oxide synthase

Laura Tedesco1, Alessandra Valerio, Cristina Cervino

  • 1Integrated Laboratories Network, Center for Study and Research on Obesity, Department of Pharmacology, Chemotherapy and Medical Toxicology, School of Medicine, Milan University, Milan, Italy.

Diabetes
|May 15, 2008
PubMed
Abstract

Insights

Cannabinoid type 1 (CB1) receptor blockade boosts mitochondrial biogenesis in white adipocytes by increasing endothelial NO synthase (eNOS) expression, preventing diet-induced fat accumulation without affecting food intake.

Area of Science:

  • Metabolism and Endocrinology
  • Cellular Biology
  • Obesity Research

Background:

  • Cannabinoid type 1 (CB1) receptor blockade reduces body weight and adiposity, but the mechanism remains unclear.
  • Endothelial NO synthase (eNOS)-produced nitric oxide (NO) is known to promote mitochondrial biogenesis and function in adipocytes.

Purpose of the Study:

  • To investigate whether CB1 receptor blockade enhances eNOS expression and mitochondrial biogenesis in white adipocytes.
  • To elucidate the role of eNOS in mediating the effects of CB1 receptor blockade on adipocyte metabolism.

Main Methods:

  • Selective pharmacological blockade of CB1 receptors using SR141716 (rimonabant) in primary mouse white adipocytes.
  • Assessment of eNOS expression and mitochondrial biogenesis in white adipose tissue (WAT) and isolated adipocytes from CB1 receptor-deficient (CB1(-/-)) mice and mice chronically treated with SR141716 on standard or high-fat diets.

Main Results:

  • SR141716 treatment upregulated eNOS expression and increased mitochondrial DNA, mRNA levels of biogenesis genes, mitochondrial mass, and function in cultured white adipocytes.
  • These effects were dependent on eNOS induction, as confirmed by siRNA-mediated knockdown.
  • In high-fat diet-fed mice, CB1 receptor deletion or SR141716 treatment normalized reduced eNOS expression and mitochondrial biogenesis in WAT, preventing weight gain and adiposity.

Conclusions:

  • CB1 receptor blockade promotes mitochondrial biogenesis in white adipocytes via eNOS induction.
  • This mechanism contributes to the prevention of high-fat diet-induced obesity and fat accumulation, independent of changes in appetite.

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