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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0116v1 203/3/327    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 Google Scholar Google Scholar Articles by Sen Gupta, P. Articles by Chapple, J P. Search for Related Content PubMed PubMed Citation Articles by Sen Gupta, P. Articles by Chapple, J P.

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

(Correspondence should be addressed to J P Chapple; Email: j.p.chapple{at}qmul.ac.uk)

Primary cilia are sensory organelles that protrude from the surface of most mammalian cell types. In humans and mice, mutations in proteins required for normal cilia function have been identified as causing a class of disorders with overlapping phenotypes known as ciliopathies. Recent evidence has linked obesity in ciliopathies to both the regulation of energy homeostasis in the hypothalamus and to adipogenesis. This article considers the role of cilia in these processes and whether cilia dysfunction may be relevant to more common forms of obesity.