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.
Original language | English |
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Pages (from-to) | 340-349 |
Number of pages | 10 |
Journal | Peptides |
Volume | 27 |
Issue number | 2 |
DOIs | |
State | Published - Feb 2006 |
Keywords
- Cholecystokinin
- Food intake
- Ghrelin
- PYY
- Proopiomelanocortin
- Satiety