CB1 cannabinoid receptor knockout in mice leads to leanness, resistance to diet-induced obesity and enhanced leptin sensitivity

By C. R. Trillou, C. Delgorge, C. Menet, M. Arnone, P. Soubrié. International Journal of Obesity, 2004

599 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Endocannabinoid activation at hepatic CB1 receptors stimulates fatty acid synthesis and contributes to diet-induced obesity. (2005, background): “Mice lacking CB1 are resistant to diet-induced obesity even though their total caloric intake is similar to that of wild-type littermates, which become obese on the same diet (16).”
Regulation, function, and dysregulation of endocannabinoids in models of adipose and beta-pancreatic cells and in obesity and hyperglycemia. (2006, background): “they consume as much food as wild types (12, 13).”
The Human Obesity Gene Map: The 2005 Update (2006, background): “9) Cnr1 6q14-q15 CNR1 Cannabinoid receptor 1 (brain), also known as CB1 receptor On standard chow at 20 weeks, the BWs and adiposity are 24% and 60% lower, respectively, than control mice Resistant to diet-induced obesity (339)”
The Endocannabinoid System as an Emerging Target of Pharmacotherapy (2006, background): “Second, CB1−/− mice are resistant to diet-induced obesity (Ravinet Trillou et al., 2004; OseiHyiaman et al., 2005b).”
The emerging role of the endocannabinoid system in endocrine regulation and energy balance. (2006, background): “By using SR141716 in DIO mice, Jbilo et al. (307) were able to reverse the phenotype of obese adipocytes at both macroscopic and genomic levels.”