Thyroid hormones influence serum leptin levels in patients with Graves' disease during suppression of beta-adrenergic receptors

Leptin is a protein product of the ob gene, mainly produced by adipocytes. Leptin is thought to play an important role in the homeostasis of body weig ht by suppressing appetite and increasing energy consumption. The aim of th is study was to investigate the possible effect of thyroid hormone on the r egulation of the leptin system during suppression of beta-adrenergic recept ors in Graves' patients. We studied 15 adult female patients with Graves' d isease. Thyroid function, serum levels of leptin, and percent body fat (%BF ) were examined at four different clinical conditions during therapy (A, un treated; B, beta-adrenergic antagonist only [A, B; hyperthyroid], C, beta-a drenergic antagonist and antithyroid drug; D, antithyroid drug only [C, D; euthyroid]). The use of beta-adrenergic antagonist significantly reduced he art rate in spite of hyperthyroid state, indicating sufficient suppression of beta-adrenergic receptors. During treatment with P-adrenergic antagonist , leptin percentage of body fat (%BF) ratio significantly decreased in euth yroid state compared to that in hyperthyroid state (from 38.7 +/- 21.3 to 1 8.1 +/- 19.3, p = 0.003). Moreover, there was a significantly positive corr elation between Delta leptin/%BF and Delta free thyroxine (FT4) (r = 0.51, p = 0.008). Under a euthyroid state induced by antithyroid drug treatment, leptin/%BF did not change in spite of withdrawal of beta-adrenergic antagon ist. Our data indicate that thyroid hormones could increase serum leptin le vel during suppression of beta-adrenergic receptors in Graves' patients. Ou r data also suggest that the beta-adrenergic action of thyroid hormones mig ht be partly mediated by regulation of leptin.