title: Prolonged high iodine intake is associated with inhibition of type 2 deiodinase activity in pituitary and elevation of serum thyrotropin levels.
abstract: Our previous epidemiological study indicated that excessive intake of iodine could potentially lead to hypothyroidism. In the present study, we aimed to investigate the time and dose effect of iodine intake on serum thyrotropin (thyroid-stimulating hormone, TSH) levels and to explore the non-autoimmune regulation of serum TSH by pituitary type 2 deiodinase (D2). A total of 360 Wistar rats were randomly divided into five groups depending on administered iodine dosages (folds of physiological dose): normal iodine (NI), 3-fold iodine (3HI), 6-fold iodine (6HI), 10-fold iodine (10HI) and 50-fold iodine (50HI). At 4, 8, 12 and 24 weeks after administration of sodium iodide, blood was collected for serum TSH measurement by chemiluminescent immunoassay. Pituitaries were also excised for measurement of TSHβ subunit expression, D2 expression and activity, monocarboxylate transporter 8 (MCT8) and thyroid hormone receptor β2 isoform (TRβ2) levels. The results showed that iodine intake of 10HI and 50HI significantly increased pituitary and serum TSH levels from 8 to 24 weeks (P < 0·05 v. NI). Excess iodine had no effect on D2 mRNA or protein expression; however, 10HI and 50HI administration significantly inhibited pituitary D2 activities from 8 to 24 weeks (P < 0·05 v. NI). Iodine had no effect on MCT8 or TRβ2 protein levels. We conclude that prolonged high iodine intake inhibits pituitary D2 activity and induces elevation of serum TSH levels. These findings may provide a potential mechanism of iodine excess-induced overt and subclinical hypothyroidism.
authors.affiliation: Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang, People's Republic of China.
authors.forename: Ningna
authors.initials: N
authors.lastname: Li
authors.forename: Yaqiu
authors.initials: Y
authors.lastname: Jiang
authors.forename: Zhongyan
authors.initials: Z
authors.lastname: Shan
authors.forename: Weiping
authors.initials: W
authors.lastname: Teng
mesh_terms: D000818:Animals; D004032:Diet / Q000009:adverse effects*; D005260:Female; D005786:Gene Expression Regulation; D007037:Hypothyroidism / Q000097:blood / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D007453:Iodide Peroxidase / Q000235:genetics / Q000378:metabolism*; D007455:Iodine / Q000008:administration & dosage / Q000009:adverse effects*; D008297:Male; D010902:Pituitary Gland / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D011499:Protein Processing, Post-Translational; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D012974:Sodium Iodide / Q000008:administration & dosage / Q000009:adverse effects; D013972:Thyrotropin / Q000097:blood*; D037322:Thyrotropin, beta Subunit / Q000235:genetics / Q000378:metabolism; D013997:Time Factors; D000097564:Iodothyronine Deiodinase Type II
chemical_list: D007453:Iodide Peroxidase; D007455:Iodine; D012333:RNA, Messenger; D012974:Sodium Iodide; D013972:Thyrotropin; D037322:Thyrotropin, beta Subunit; D000097564:Iodothyronine Deiodinase Type II