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Cannabinoid Receptor 2 as Antiobesity Target: Inflammation, Fat Storage, and Browning Modulation

Francesca Rossi1, Giulia Bellini1, Livio Luongo1

  • 1Department of Women, Child and General and Specialist Surgery (F.R., I.M., A.G., B.N., L.P., E.M.d.G.) and Department of Experimental Medicine (G.B., L.L., I.M., C.T., S.M.), Division of Pharmacology Leonardo Donatelli, The Second University of Naples, 80138 Naples, Italy; The Endocannabinoid Research Group (L.L., S.M.), 80078 Pozzuoli, Naples, Italy; Division of General and Obesity Surgery (S.T., L.D.), The Second University of Naples, 80131 Naples, Italy; Department of Onco-Hematology (M.E.B., A.C., F.L.), Istituto di Ricovero e Cura a Caarattere Scientifico Bambino Gesù Children's Hospital, 00165 Rome, Italy; and University of Pavia (F.L.), 27100 Pavia, Italy.

The Journal of Clinical Endocrinology and Metabolism
|June 14, 2016
PubMed
Abstract

Insights

The less-functional CB2-R63 variant is linked to childhood obesity. Targeting the CB2 receptor may offer a new therapeutic strategy for managing obesity and its associated inflammatory effects.

Area of Science:

  • Endocrinology and Metabolism
  • Molecular Biology
  • Genetics

Background:

  • Obesity is linked to low-grade inflammation and altered adipose tissue (ADP) characteristics.
  • The Cannabinoid Receptor 2 (CB2) plays a role in regulating food intake and has shown anti-obesity effects in animal models.
  • A specific variant, CB2-Q63R, is associated with reduced CB2 receptor function.

Purpose of the Study:

  • To investigate the impact of the CB2 receptor on childhood obesity.
  • To analyze the influence of CB2 receptor modulation on adipocyte activity and morphology.
  • To assess the role of the CB2-Q63R variant in obese children.

Main Methods:

  • Analysis of the CB2-Q63R variant in 501 obese Italian children.
  • In vitro studies using adipocytes derived from mesenchymal stem cells and adipose tissue biopsies from lean and obese adults.
  • Investigation of inflammatory stimuli and selective CB2 receptor agonists/antagonists (AM630, JWH-133) effects on adipocytes.

Main Results:

  • The less-functional CB2-R63 variant showed a significant association with higher body mass index z-scores in children.
  • CB2 receptor blockade increased inflammatory adipokine release, fat storage, and reduced adipose tissue browning.
  • CB2 receptor stimulation with JWH-133 reversed obesity-related effects, including increased browning and reduced inflammation.

Conclusions:

  • The CB2 receptor is a potential pharmacological target for obesity treatment.
  • Modulating CB2 receptor activity can influence adipocyte function, inflammation, and energy metabolism.
  • The CB2-Q63R variant may contribute to the pathophysiology of obesity.

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