Hyperphagia and Obesity in 5HT2CReceptor Knockout Mouse

Serotonin modulates numerous autonomic functions. It acts through the activation of a large family of G-protein-coupled-receptor subtypes that are widely expressed throughout the brain. The complexity of this signaling system and the paucity of selective drugs have made it especially difficult to define specific roles for 5-HT-receptor subtypes. Mutant mice lacking functional 5-HT2C receptors have been generated to elucidate the physiological function of this widely expressed receptor (156,157). Unexpectedly, 5-HT2C receptor-deficient mice display substantial overweight as a result of increased appetite. This obesity is characterized by leptin and insulin resistance, impaired glucose tolerance, and increased responsiveness to high-fat feeding. Thus, these mutant mice have established a role for the 5-HT2C receptor in the serotonergic control of feeding and energy expenditure. These findings also demonstrate a dissociation of serotonin and leptin signaling in the regulation of feeding, and indicate that a perturbation of brain serotonin systems can predispose to eating disorders, obesity, and type 2 diabetes (156,157) (see Table 2).

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