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

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Wheeldon, N.M. et al.

Beta-adrenoceptor subtypes mediating the metabolic effects of BRL 35135 in man.

1. The aim of the present study was to evaluate the metabolic responses produced in man by the beta 3-adrenoceptor agonist BRL 35135, and to determine which of these responses are beta 3-, rather than beta 1- or beta 2-, mediated. 2. Eight normal male subjects received single oral doses of BRL 35135 (8 mg) or the selective beta 2-adrenoceptor agonist salbutamol (8 mg) after pretreatment with placebo, bisoprolol (5 mg) as a selective beta 1-antagonist or nadolol (20 mg) to block beta 1- and beta 2-, but not beta 3-adrenoceptors. 3. BRL 35135 and salbutamol produced a significant fall in serum potassium concentration compared with placebo, in keeping with beta 2-adrenoceptor stimulation. Both drugs also produced a significant increase in serum glucose, insulin and lactate concentrations, which mirrored the hypokalaemic response, being unaffected by selective beta 1-blockade (bisoprolol), but completely blocked by nadolol. BRL 35135 (but not salbutamol) also produced a significant rise in serum free fatty acid and glycerol concentrations, which appeared to be beta 2-mediated. 4. A significant increase in basal metabolic rate occurred with both BRL 35135 and salbutamol. In the case of salbutamol, this effect appeared to be mediated solely by beta 2-adrenoceptors, whereas BRL 35135 produced a thermogenic response which could only be partially accounted for by a combination of beta 1- and beta 2-adrenoceptor stimulation. 5. These results infer the possibility of thermogenic beta 3-adrenoceptors in man, although these do not appear to be involved in the control of carbohydrate or fat metabolism.[1]

References

Beta-adrenoceptor subtypes mediating the metabolic effects of BRL 35135 in man. Wheeldon, N.M., McDevitt, D.G., McFarlane, L.C., Lipworth, B.J. Clin. Sci. (1994) [Pubmed]

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