Regulation of adipose tissue metabolism via adrenergic mechanisms: actions of alpha-adrenoceptor agonists on lipolysis in hamster fat cells.

The effects of two alpha-1-adrenergic agonists (phenylephrine, cirazoline) and two alpha-2-adrenergic agonists (clonidine, guanabenz) were investigated on lipolysis stimulated by noradrenaline, isoprenaline, dibutyryl cyclic AMP (dbc AMP) or methylisobutylxanthine (MIX) in hamster adipose cells, in vitro. Phenylephrine enhanced basal lipolysis and that stimulated by dbc AMP and MIX, whereas cirazoline showed no measurable effects. Clonidine produced a slight but significant decrease of basal lipolysis. Both clonidine and guanabenz (from 10(-7) M) provoked a similar and clear inhibition (50-60 per cent) of MIX-stimulated lipolysis, compatible with the view that the alpha-adrenergic receptor of the hamster white fat cell is of the alpha-2 type. Noradrenaline-stimulated lipolysis was unaffect and isoprenaline-stimulated lipolysis moderately inhibited, by clonidine and guanabenz. Since the beta-adrenergic lipolytic effects of noradrenaline are known to be associated with a simultaneous alpha-adrenergic inhibitory stimulus, and one possible explanation of the but moderate inhibition of isoprenaline-induced lipolysis could be simultaneous beta-adrenergic stimulation (resulting in lipolysis), and alpha-adrenergic stimulation (inhibition of lipolysis), as with noradrenaline, the nature of isoprenaline as a pure beta-adrenergic agonist requires clarification.