Recent studies suggest that thermogenesis in brown adipose tissue has an important role in the regulation of energy balance^1–7. Thermogenesis is effected by noradrenaline released from sympathetic nerve endings; the noradrenaline stimulates β;-adrenoceptors, causing lipolysis, and the released fatty acids then promote the uncoupling of oxidative phosphorylation from electron transport^8,9. It has been widely accepted^10–13 that mammalian β-adrenoceptors exist as two subtypes, β₁ and β₂ (ref. 14), and rat brown adipocyte β-adrenoceptors have been classed as β₁ (refs 15–17) or as a mixed β₁/β₂ population¹⁸. The β₁ subtype predominates in atria, whereas the β₂ subtype predominates in trachea. However, we have now found a novel group of β-adrenoceptor agonists that selectively stimulate lipolysis in brown adipocytes. In contrast, isoprenaline, fenoterol and salbutamol are less potent as stimulants of lipolysis than as stimulants of atrial rate or tracheal relaxation. Therefore, β-adrenoceptors in rat brown adipocytes are of neither the β₁ nor β₂ subtypes. Compounds that selectively stimulate brown adipocyte β-adrenoceptors should have potential as thermogenic anti-obesity agents and this has been demonstrated with BRL 26830A, BRL 33725A and BRL 35135A.