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3-Adrenergic Receptor Activation
1 Center for Integrative Metabolic and Endocrine Reseach, Departments of Psychiatry and Pathology, Wayne State University School of Medicine, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: jgranne{at}med.wayne.edu.
Selective agonists of 
3-adrenergic receptors (Adrb3) agonists exert potent anti-diabetes effects in rodent models when given chronically, yet the mechanisms involved are poorly understood. A salient feature of chronic Adrb3 activation is pronounced remodeling of white adipose tissue (WAT) which includes mitochondrial biogenesis and elevation of metabolic rate. To gain insights into potential mechanisms underlying WAT remodeling, the time course of remodeling induced by the Adrb3 agonist CL 316,243 (CL) was analyzed using histological, physiological and global gene profiling approaches. The results indicate that continuous CL treatment induced a transient proinflammatory response that was followed by cellular proliferation among stromal cells and multilocular adipoctyes. CL treatment strongly fragmented the central lipid storage droplet of mature adipocytes and induced mitochondrial biogenesis within these cells. Mitochondrial biogenesis was correlated with the upregulation of genes involved in fatty acid oxidation and mitochondrial electron transport activity. The elevated catabolic activity of WAT was temporally correlated with upregulation of peroxisome proliferators activated receptor alpha and its target genes, suggesting involvement of this transcription factor in coordinating the gene program that elevates WAT catabolic activity.
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