Anti-obesity efficacy of LH-21, a cannabinoid CB(1) receptor antagonist with poor brain penetration, in diet-induced obese rats

Br J Pharmacol. 2012 Apr;165(7):2274-91. doi: 10.1111/j.1476-5381.2011.01698.x.

Abstract

Background and purpose: Peripheral blockade of cannabinoid CB(1) receptors has been proposed as a safe and effective therapy against obesity, putatively devoid of the adverse psychiatric side effects of centrally acting CB(1) receptor antagonists. In this study we analysed the effects of LH-21, a peripherally acting neutral cannabinoid receptor antagonist with poor brain penetration, in an animal model of diet-induced obesity.

Experimental approach: To induce obesity, male Wistar rats were fed a high-fat diet (HFD; 60 kcal% fat) whereas controls received a standard diet (SD; 10 kcal% fat). Following 10 weeks of feeding, animals received a daily i.p. injection of vehicle or 3 mg·kg(-1) LH-21 for 10 days. Plasma and liver samples were used for biochemical analyses whereas visceral fat-pad samples were analysed for lipid metabolism gene expression using real-time RT-PCR. In addition, the potential of LH-21 to interact with hepatic cytochrome P450 isoforms and cardiac human Ether-à-go-go Related Gene (hERG) channels was evaluated.

Key results: LH-21 reduced feeding and body weight gain in HFD-fed animals compared with the control group fed SD. In adipose tissue, this effect was associated with decreased gene expression of: (i) leptin; (ii) lipogenic enzymes, including SCD-1; (iii) CB(1) receptors; and (iv) both PPARα and PPARγ. Although there were no significant differences in plasma parameters between HFD- and SD-fed rats, LH-21 did not seem to induce hepatic, cardiac or renal toxicity.

Conclusions and implications: These results support the hypothesis that treatment with the peripherally neutral acting CB(1) receptor antagonist, LH-21, may promote weight loss through modulation of visceral adipose tissue.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Obesity Agents / pharmacokinetics
  • Anti-Obesity Agents / pharmacology*
  • Anti-Obesity Agents / toxicity
  • Brain / metabolism
  • Diet, High-Fat / adverse effects
  • ERG1 Potassium Channel
  • Eating / drug effects
  • Ether-A-Go-Go Potassium Channels / drug effects
  • Gene Expression / drug effects
  • HEK293 Cells
  • Humans
  • Intra-Abdominal Fat / drug effects
  • Intra-Abdominal Fat / metabolism
  • Leptin / genetics
  • Lipogenesis / drug effects
  • Lipogenesis / genetics
  • Liver / drug effects
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Knockout
  • Obesity / drug therapy*
  • Obesity / etiology
  • Obesity / genetics
  • Obesity / metabolism
  • PPAR alpha / deficiency
  • PPAR alpha / genetics
  • PPAR gamma / genetics
  • Rats
  • Rats, Wistar
  • Receptor, Cannabinoid, CB1 / antagonists & inhibitors*
  • Receptor, Cannabinoid, CB1 / genetics
  • Triazoles / pharmacokinetics
  • Triazoles / pharmacology*
  • Triazoles / toxicity
  • Weight Gain / drug effects

Substances

  • 5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-3-hexyl-1H-1,2,4-triazole
  • Anti-Obesity Agents
  • ERG1 Potassium Channel
  • Ether-A-Go-Go Potassium Channels
  • KCNH2 protein, human
  • Leptin
  • PPAR alpha
  • PPAR gamma
  • Receptor, Cannabinoid, CB1
  • Triazoles