Ciliary dysfunction and obesity
Article first published online: 23 NOV 2009
© 2009 John Wiley & Sons A/S
Volume 77, Issue 1, pages 18–27, January 2010
How to Cite
Mok, C., Héon, E. and Zhen, M. (2010), Ciliary dysfunction and obesity. Clinical Genetics, 77: 18–27. doi: 10.1111/j.1399-0004.2009.01305.x
- Issue published online: 21 DEC 2009
- Article first published online: 23 NOV 2009
- Received 14 August 2009, revised and accepted for publication 18 August 2009
- Bardet-Biedl syndrome;
- primary cilium;
Mok CA, Héon E, Zhen M. Ciliary dysfunction and obesity.
Obesity associates with increased health risks such as heart disease, stroke and diabetes. The steady rise in the obese population worldwide poses an increasing burden on health systems. Genetic factors contribute to the development of obesity, and the elucidation of their physiological functions helps to understand the cause, and improve the prevention, diagnosis and treatment for this disorder. Primary cilia are evolutionarily conserved organelles whose dysfunctions lead to human disorders now defined as ciliopathies. Human ciliopathies present pleiotropic and overlapping phenotypes that often include retinal degeneration, cystic renal anomalies and obesity. Increasing evidence implicates an intriguing involvement of cilia in lipid/energy homeostasis. Here we discuss recent studies in support of the key roles of ciliary genes in the development and pathology of obesity in various animal models. Genes affecting ciliary development and function may pose promising candidate underlying genetic factors that contribute to the development of common obesity.