Jerzy R. Szewczyk and Chris Laudeman Pages 837 - 854 ( 18 )
Almost 30 years have passed since Gibbs, Young, and Smith demonstrated the ability of exogenously administered cholecystokinin (CCK) to inhibit food intake in rats. This observation was the beginning of very extensive studies into the role CCK plays in the regulation of food intake in mammals. CCK is a brain-gut peptide, which exists in multiple forms. CCK peptides exert their action on two distinct receptor subtypes: CCK-A (Alimentary) now called the CCK1R, mostly expressed peripherally, and CCK-B (Brain), renamed the CCK2R, which is primarily present in the brain. Through the use of subtypeselective agonists and antagonists for the CCK receptor, it was determined that the effect of CCK on feeding was dependent on agonist induced activation of peripheral CCK1 receptors. This discovery was followed by intense research with the goal of identifying small molecule agonists on the CCK1 receptor as potentially useful agents for the treatment of obesity. This review will attempt to summarize the results of this research.
cholecystokinin, cck1r, obesity, satiety, paracrine, benzodiazepines, peptides
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