Reduction of increased levels of blood glycerol and ketone bodies by propranolol in human hyperthyroidism: Role of the fall of the triiodothyronine level

Hyperthyroid patients in the postabsorptive state have elevated levels of blood glycerol and ketone bodies (KB): this is believed to be due to increased lipolysis and ketogenesis. These increased glycerol and KB levels return toward normal after oral propranolol administration. In order to investigate the mechanism of action of propranolol in hyperthyroid patients, we compared the effects of the oral administration of propranolol with those of timolol, propylthiouracil (PTU), and a placebo. The placebo had no effect. The free thyroxine index, immunoreactive insulin level and glucagon level were not modified by propranolol, timolol, or PTU. Propranolol decreased the pulse rate (P < 0.01) and the levels of serum triiodothyronine (T₃; P < 0.05), blood glycerol (P < 0.01), and KB (P < 0.01). Like propanolol, timolol decreased the pulse rate (P < 0.01) but had no effect on the T₃, glycerol, or KB levels. Propylthiouracil did not modify the pulse rate, but like propanolol, it decreased the T₃ (P < 0.05), glycerol (P < 0.01) and KB (P < 0.01) levels. These results suggest that the metabolic actions of propranolol are not caused by its hemodynamic effects nor its beta-blocking properties but are mediated by the decrease of the T₃ level.