Thyroid function ultimately depends on appropriate iodine supply to the gland. Thyroid hormone deiodination is an intrinsic component of the thyroid hormone homeostasis. Type Ⅰ iodothyronine deiodinase (D1) plays an important role in thyroid hormone metabolism and has close relationship with thyroid function. Based on successfully establishing animal models of iodine deficiency and iodine excess in Babl/c mice (Babl/c mice were randomly divided into five groups: low iodine (LI), normal iodine (NI), five-fold iodine (5HI) , ten-fold iodine (10HI) and fifty-fold iodine (50HI) group. Three months and six months after admistration, they were sacrificed and thyroids were excised), the expression level of D1 mRNA were examined by using real time quantitative PCR method. D1 activity was analyzed by ¹²⁵I-rT₃ as substrate combined with ion-exchange chromatography. The thyroid hormone was measured with radioimmunoassay method. The data revealed that in the case of iodine deficiency, both D1 mRNA expression and D1 activity was greatly increased(compared with NI groups, P < 0.01). T₃ and T₄ in thyroid tissue was significantly decreased, but T₃ / T₄ was increased (P < 0.01). On the other hand, when faced to iodine excess, D1 mRNA expression was reduced (There was a tendency of decreasing in D1 mRNA expression in all HI groups compared with NI group, significant difference was found in 5HI and 50HI at 6 months ), while there was no remarkable effect on D1 activity. The thyroid hormone assay showed that T₃ / T₄ was decreased. In conclusion, D1 is a critical factor in the regulation mechanism of thyroid function. The up-regulated mRNA expression and activity under the state of iodine deficiency will improve the conversion of T₄ to T₃ to maintain the normal thyroid function. The inhibition of D1 expression induced by iodine excess may be taken as an effective way to protect organism from impairment caused by too much T₃.