Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2008407 | Peptides | 2006 | 10 Pages |
Abstract
Genetic and pharmacological studies have shown that the central melanocortin system plays a critical role in the regulation of energy homeostasis. Animals and humans with defects in the central melanocortin system display a characteristic melanocortin obesity phenotype typified by increased adiposity, hyperphagia, metabolic defects and increased linear growth. In addition to interacting with long-term regulators of energy homeostasis such as leptin, more recent data suggest that the central melanocortin system also responds to gut-released peptides involved in mediating satiety. In this review, we discuss the interactions between these systems, with particular emphasis on cholecystokinin (CCK), ghrelin and PYY3–36.
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Authors
Kate L.J. Ellacott, Ilia G. Halatchev, Roger D. Cone,