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This version published online on July 8, 2004
Molecular Endocrinology, doi:10.1210/me.2004-0193
A more recent version of this article appeared on September 1, 2004
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Submitted on May 7, 2004
Accepted on July 1, 2004

Learning new tricks from old dogs: {beta}-adrenergic receptors teach new lessons on firing up adipose tissue metabolism

Sheila Collins*, Wenhong Cao, and Jacques Robidoux

CIIT Centers for Health Research, Research Triangle Park, NC 27709 and Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710

* To whom correspondence should be addressed. E-mail: scollins{at}ciit.org.

The three {beta}-adrenergic receptor ({beta}AR) subtypes ({beta}1AR, {beta}2AR {beta}3AR) are members of the large family of G protein-coupled receptors, each of which is coupled to G{alpha}s and increases in intracellular cAMP levels. In white adipose tissues (WAT), catecholamine activation of the {beta}ARs leads to the mobilization of stored fatty acids and regulates release of several adipokines, while in brown adipose tissue (BAT) they stimulate the specialized process of adaptative non-shivering thermogenesis. Noteworthy, in most models of obesity the {beta}AR system is dysfunctional and its ability to stimulate lipolysis and thermogenesis are both impaired. Nevertheless, selective agonists for the {beta}3AR, a subtype that is found predominantly in adipocytes, have been able to prevent or reverse obesity and accompanying insulin resistance in animal models. Whether this is a viable therapeutic option for human obesity is much debated with regard to the existence of brown adipocytes in humans or their ability to be recruited. Nevertheless, probing the physiological changes in adrenoceptor function in rodent obesity, as well as the process by which {beta}3AR agonists promote a thermogenic shift in fuel utilization, have yielded unexpected new insights into {beta}AR signaling and adipocyte physiology. These include the recent discovery of an essential role of p38 MAP kinase in mediating adaptative thermogenesis, as well as the accessory role of the ERK MAP kinase pathway for the control of lipolysis. Since these metabolic events were traditionally ascribed solely to the cAMP/ protein kinase A system, the integration of these signaling mechanisms may pose new therapeutic directions in the quest to counter the obesity epidemic in our midst.




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