Roles of alpha and beta adrenergic receptors in control of glucose oxidation in hamster epididymal adipocytes

Oxidation of ¹⁴C]glucose in isolated epididymal adipocytes from Golden hamsters was stimulated by isoproterenol and norepinephrine, which all interact with β-adrenergic receptors and by adrenorticotrophic hormone. In contrast α-receptor agonists, such as phenylephrine, methoxamine or clonidine did not increase basal glucose oxidation. The β-adrenergic blocking drug propranolol inhibited both lipolysis and glucose oxidation when these had been stimulated by isoproterenol, ephinephrine and phenoxybenzamine did not the α-adrenergic blocking drugs phentolamine and phenoxybenzamine did not influence lipolysis or glucose oxidation when isoproterenol provided the stimulus and increased both liposlysis and glucose metabolism in the presence of either epinephrine or norepinephrine. All α-adrenergic agonists tested (phenylephrine, methoxamine and clonidine) lowered liposlysis and glucose oxidation in isolated adipocytes exposed to isoproterenol. However, when adrenorcortropin provided the stimulus for glucose oxidation and lipolysis, only clonidine produced a significant reduction in lipolysis and glucose oxidation. None of the α-agonists influenced glucose metabolism which had been increased by insulin. These data confirm the presence of both α and β adrenergic receptors on hamster epididymal adipocytes and suggests that they exert antagonistic influences on lipolysis and glucose oxidation. These data are also consistent with the view that adrenergic stimulation of glucose oxidation and lipolysis in adipocytes are both mediated through β receptors.