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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0056v1 202/2/191    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Kola, B. Articles by Korbonits, M. Search for Related Content PubMed PubMed Citation Articles by Kola, B. Articles by Korbonits, M.

Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Centre for Endocrinology, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK

(Correspondence should be addressed to M Korbonits; Email: m.korbonits{at}qmul.ac.uk)

Ghrelin, a hormone primarily produced by the stomach, has a wide range of metabolic and non-metabolic effects. It also stimulates food intake through activation of various hypothalamic and brain stem neurons. A series of recent studies have explored the intracellular mechanisms of the appetite-inducing effect of ghrelin in the hypothalamus, shedding light on the intricate mechanisms of appetite regulation. AMP-activated protein kinase (AMPK) is a key metabolic enzyme involved in appetite regulation. Calmodulin kinase kinase 2 (CaMKK2) has been identified as an upstream kinase of AMPK and a key mediator in the effect of ghrelin on AMPK activity. The fatty acid pathway, hypothalamic mitochondrial respiration, and uncoupling protein 2 have been outlined as downstream targets of AMPK and mediators of ghrelin's appetite stimulating effect. This short overview summarises the present data in this field.