The relation between thyrotoxicosis, the clinical syndrome resulting from 
exposure to excessive thyroid hormone concentrations, and the sympathetic 
nervous system remains enigmatic. Nevertheless, beta-adrenergic blockers are 
widely used to manage severe thyrotoxicosis. Recent experiments show that the 
effects of thyrotoxicosis on hepatic glucose production and insulin sensitivity 
can be modulated by selective hepatic sympathetic and parasympathetic 
denervation. Indeed, thyroid hormone stimulates hepatic glucose production via a 
sympathetic pathway, a novel central pathway for thyroid hormone action. Rodent 
studies suggest that similar neural routes exist for thyroid hormone analogues 
(e.g. thyronamines). Further elucidation of central effects of thyroid hormone 
on autonomic outflow to metabolic organs, including the thyroid and brown 
adipose tissue, will add to our understanding of hyperthyroidism.