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Journal of Obesity
Volume 2011, Article ID 609485, 10 pages
Review Article

Relationships of Adrenoceptor Polymorphisms with Obesity

1Nucleus Network, Ltd, Baker IDI Heart and Diabetes Research Institute, 89 Commercial Road, Melbourne, VIC 3004, Australia
2Human Neurotransmitter Laboratory, Baker IDI Heart and Diabetes Research Institute, Melbourne, VIC 3004, Australia

Received 24 November 2010; Accepted 7 February 2011

Academic Editor: Eric Doucet

Copyright © 2011 Kazuko Masuo and Gavin W. Lambert. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Obesity, hypertension, and type 2 diabetes are rapidly growing public health problems. Heightened sympathetic nerve activity is a well-established observation in obesity, hypertension, and type 2 diabetes. Human obesity, hypertension, and diabetes have strong genetic as well as environmental determinants. Reduced energy expenditure and resting metabolic rate are predictive of weight gain, and the sympathetic nervous system participates in regulating energy balance through thermogenesis. The thermogenic effects of catecholamines in obesity are mainly mediated via the β2, and β3-adrenergic receptors in humans. Further, β2-adrenoceptors importantly influence vascular reactivity and may regulate blood pressure. β-adrenoceptor polymorphisms have also been associated with adrenoceptor desensitization, increased adiposity, insulin resistance, and enhanced sympathetic nervous activity. Many epidemiological studies have shown strong relationships between adrenoceptor polymorphisms and obesity, but the observations have been discordant. This paper will discuss the current topics involving the influence of the sympathetic nervous system and β2- and β3-adrenoceptor polymorphisms in obesity.