Endocannabinoids are natural cannabis-like proteins that can stimulate appetite and regulate fat metabolism by binding to receptors called CB1. Drugs that block these receptors may be useful for treating obesity by suppressing appetite and food intake. In a new study appearing in the May 2 print issue of The Journal of Clinical Investigation, George Kunos and colleagues from the NIH examine the possible role of the liver as a target of the metabolic actions of endocannabinoids.

The authors find that liver cells express CB1 and when stimulated, these cells activate a signaling pathway that ultimately increases fatty acid synthesis. The cellular proteins that are activated in the liver upon CB1 stimulation are the same as those known to be activated in the brain and thus may be a common molecular target for metabolic regulation and appetite control.

In an accompanying commentary, Aron Lichtman and Benjamin Cravatt write, "A particularly provocative implication of the workis that endocannabinoid-mediated modulation of lipogenesis in the liver may contribute to the development of fatty liver and obesity. Targeting these pathways could promote sustained weight loss and favorable serum lipid profiles in obese patients"

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Contact: Stacie Bloom
press_releases@the-jci.org
212 342-4159
Journal of Clinical Investigation
2-May-2005

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