The effect of thyroid hormone on size of fat depots accounts for most of the changes in leptin mRNA and serum levels in the rat

The physiological consequences and mechanism(s) for thyroid hormone-induced alterations in serum leptin are not known. To address this, leptin express ion in rats was evaluated in relationship to food intake, fat mass, and bod y temperature in rats with pharmacologically altered thyroid status. Total body weight, food intake, and temperature were decreased in hypothyroid rat s. Fat weight was decreased in both chronically hypothyroid and hyperthyroi d rats (rt = 6/group). Serum leptin was linearly correlated with fat weight , epididymal and retroperitoneal fat leptin mRNA concentration, but not tot al body weight. Serum leptin was decreased in the chronically hyperthyroid rats. When fat weight was used as a covariant, serum leptin was not differe nt between the three groups. Epididymal fat leptin mRNA was higher in euthy roid (n = 7) than in hypothyroid and hyperthyroid rats. Retroperitoneal fat leptin mRNA was not affected by thyroid status. A positive linear relation ship between food intake and free triiodothyronine (FT3) index was observed , but not between food intake and serum leptin alone. In a time course stud y, serum leptin, epididymal fat leptin mRNA content, and fat weight did not change within 24 hours of high-dose triiodothyronine (T-3) (n = 6/group), but both temperature and epididymal fat S14 mRNA content rapidly increased. These findings demonstrate that thyroid state influences circulating lepti n levels, but primarily does so indirectly through the regulation of fat ma ss. Leptin does not influence core body temperature across thyroidal state. Finally, thyroid state is more important to regulate food intake, through an as yet undefined mechanism, than are thyroid state-associated changes in serum leptin.