Allen E M, Appel M C, Braverman L E
Endocrinology. 1987 Aug;121(2):481-5. doi: 10.1210/endo-121-2-481.
We have recently reported that iodine administration (0.05% iodine in drinking water) to weanling, diabetes mellitus- and lymphocytic thyroiditis (LT)-prone Biobreeding Worcester (BB/W) rats strikingly increases the incidence of LT without occurrence of iodine-induced hypothyroidism, which frequently results when excess iodine is administered to euthyroid patients with Hashimoto's thyroiditis. Since hypothyroidism did not occur in the iodine-treated BB/W rats, hemithyroidectomy was carried out in 30-day-old BB/W rats to increase thyroid mass and functional reserve. Iodine administration for 60 days markedly increased antithyroglobulin antibodies (0.40 +/- 0.08 vs. 0.15 +/- 0.06 OD; P less than 0.02), the incidence of LT (68% vs. 13%; P less than 0.001), and thyroid weight of the residual lobe (10.5 +/- 0.7 vs. 6.3 +/- 0.3 mg/100 g BW; P less than 0.001) and induced hypothyroidism (T4, 2.5 +/- 0.2 vs. 3.0 micrograms/dL; P less than 0.05; T3, 25.1 +/- 1.9 vs. 37.5 ng/dL; P less than 0.001; TSH, 252 +/- 49 vs. 61 +/- 14 microU/mL; P less than 0.02). Hypothyroidism in the iodine-treated rats occurred primarily in those with LT. Similar studies were carried out in the non-diabetes mellitus-, non-LT-prone, genetically equivalent BB/W rats (W-line), the parent strain Wistar-Furth rats, and Sprague-Dawley rats. Iodine administration did not induce LT or antithyroglobulin antibodies in these three strains and did not affect thyroid function in Wistar-Furth and Sprague-Dawley rats. However, in the W-line rats, iodine excess did induce thyroid enlargement in the residual lobe (8.4 +/- 0.2 vs. 6.4 +/- 0.2 mg/100 g BW; P less than 0.001), a decrease in serum T3 (71.5 +/- 2.9 vs. 86.0 +/- 2.5 ng/dL; P less than 0.001), and an increase in serum TSH (344 +/- 65 vs. 69 +/- 6.0 microU/mL; P less than 0.001). It is evident, therefore, that hemithyroidectomy in BB/W rats sufficiently reduces functioning thyroid tissue, resulting in iodine-induced LT and hypothyroidism, similar to iodine-induced hypothyroidism in euthyroid patients with Hashimoto's thyroiditis. It is unclear, however, why iodine administration also induced hypothyroidism in hemithyroidectomized, genetically similar, W-line rats in the absence of LT. This observation suggests that iodine-induced hypothyroidism in rats may be genetically determined.
我们最近报告称,给断乳期、易患糖尿病和淋巴细胞性甲状腺炎(LT)的Biobreeding Worcester(BB/W)大鼠饮用含碘(0.05%碘于饮用水中)的水,显著增加了LT的发病率,且未出现碘诱导的甲状腺功能减退,而给患有桥本甲状腺炎的甲状腺功能正常的患者过量补碘时,常常会出现这种情况。由于接受碘治疗的BB/W大鼠未发生甲状腺功能减退,故对30日龄的BB/W大鼠进行了甲状腺半切除术,以增加甲状腺质量和功能储备。给予碘60天显著增加了抗甲状腺球蛋白抗体(0.40±0.08对0.15±0.06 OD;P<0.02)、LT的发病率(68%对13%;P<0.001)以及残余叶的甲状腺重量(10.5±0.7对6.3±0.3 mg/100 g体重;P<0.001),并诱发了甲状腺功能减退(T4,2.5±0.2对3.0μg/dL;P<0.05;T3,25.1±1.9对37.5 ng/dL;P<0.001;TSH,252±49对61±14μU/mL;P<0.02)。碘治疗大鼠的甲状腺功能减退主要发生在患有LT的大鼠中。在非糖尿病、非LT易患、基因等同的BB/W大鼠(W系)、亲代品系Wistar-Furth大鼠和Sprague-Dawley大鼠中进行了类似研究。给予碘并未在这三个品系中诱发LT或抗甲状腺球蛋白抗体,且对Wistar-Furth大鼠和Sprague-Dawley大鼠的甲状腺功能无影响。然而,在W系大鼠中,碘过量确实诱发了残余叶甲状腺肿大(8.4±0.2对6.4±0.2 mg/100 g体重;P<0.001)、血清T3降低(71.5±2.9对86.0±2.5 ng/dL;P<0.001)以及血清TSH升高(344±65对69±6.0μU/mL;P<0.001)。因此,很明显,BB/W大鼠的甲状腺半切除术充分减少了有功能的甲状腺组织,导致碘诱导的LT和甲状腺功能减退,类似于患有桥本甲状腺炎的甲状腺功能正常的患者中碘诱导的甲状腺功能减退。然而,尚不清楚为何在无LT的情况下,给予碘也会在接受甲状腺半切除术、基因相似的W系大鼠中诱发甲状腺功能减退。这一观察结果表明,大鼠中碘诱导的甲状腺功能减退可能由基因决定。