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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

A selective human beta3 adrenergic receptor agonist increases metabolic rate in rhesus monkeys.

Activation of beta3 adrenergic receptors on the surface of adipocytes leads to increases in intracellular cAMP and stimulation of lipolysis. In brown adipose tissue, this serves to up-regulate and activate the mitochondrial uncoupling protein 1, which mediates a proton conductance pathway that uncouples oxidative phosphorylation, leading to a net increase in energy expenditure. While chronic treatment with beta3 agonists in nonprimate species leads to uncoupling protein 1 up-regulation and weight loss, the relevance of this mechanism to energy metabolism in primates, which have much lower levels of brown adipose tissue, has been questioned. With the discovery of L-755,507, a potent and selective partial agonist for both human and rhesus beta3 receptors, we now demonstrate that acute exposure of rhesus monkeys to a beta3 agonist elicits lipolysis and metabolic rate elevation, and that chronic exposure increases uncoupling protein 1 expression in rhesus brown adipose tissue. These data suggest a role for beta3 agonists in the treatment of human obesity.[1]


  1. A selective human beta3 adrenergic receptor agonist increases metabolic rate in rhesus monkeys. Fisher, M.H., Amend, A.M., Bach, T.J., Barker, J.M., Brady, E.J., Candelore, M.R., Carroll, D., Cascieri, M.A., Chiu, S.H., Deng, L., Forrest, M.J., Hegarty-Friscino, B., Guan, X.M., Hom, G.J., Hutchins, J.E., Kelly, L.J., Mathvink, R.J., Metzger, J.M., Miller, R.R., Ok, H.O., Parmee, E.R., Saperstein, R., Strader, C.D., Stearns, R.A., MacIntyre, D.E. J. Clin. Invest. (1998) [Pubmed]
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