不同摄碘水平的哺乳期母鼠与其仔鼠碘代谢及甲状腺功能和形态变化的对比研究

目的通过观察不同碘摄入水平的哺乳期母鼠及其仔鼠的碘代谢、甲状腺功能和形态的变化,探讨高碘摄入的亲代对其子代大鼠的保护作用。方法选用Wistar大鼠给予不同剂量的碘酸钾,喂养3个月后交配,观察母鼠乳汁碘及其与生后14日龄仔鼠的尿碘、甲状腺激素、甲状腺组织学变化等指标。结果(1)低碘组母鼠和仔鼠尿碘、血清T4水平均明显降低;母鼠甲状腺显著肿大,仔鼠甲状腺肿大虽不明显,但有明显的滤泡增生。(2)各高碘组母鼠尿碘水平随碘摄入量的增加而增加,二者呈平行关系,而乳汁含碘量仅表现为轻度升高,与碘摄入量不呈平行关系;各高碘组仔鼠的尿碘水平与母鼠乳汁含碘量呈平行关系。(3)各高碘组母鼠的血清T4随碘摄入量增加而降低,但未见甲状腺肿大,组织学表现为胶质蓄积性大滤泡增多和小滤泡增生同时存在,在50倍和100倍高碘组滤泡增生更明显;各高碘组仔鼠血清T4随碘摄入量的增加变化不明显,未出现母鼠发生的甲状腺功能减退(甲减)现象,甲状腺仅在100倍高碘组表现出轻度的滤泡增生。结论无论亲代和子代大鼠摄入的过量碘大部分从尿中排出;高碘摄入的亲代可能通过乳腺的调节作用减少了哺乳期子代对碘的摄入量;长期摄入过量碘的母鼠发生了甲状腺功能低下,但哺乳期仔鼠甲状腺功能基本正常;结果提示高碘摄入的亲代对其子代具有一定的保护作用。

A comparative study on iodine metabolism, thyroid function and morphological changes between lactating mother rats and their offspring with different iodine intake

Objective To study whether the lactating mothers with high iodine intake have a potential role to protect their offspring from iodine excess, and to observe the iodine metabolism, thyroid function and thyroid morphology in maternal rats and their offspring. Methods Wistar rats were fed on a diet with different doses of KIO3 for 3 months and then mated randomly. The lactating mothers and their 14 days old offspring were studied in our study. The urinary iodine, iodine in breast milk, serum T4 and thyroid morphological changes were observed. Results (1) Urinary iodine and serum T4 level in LI mothers and their pups were lower than that in all other groups (P < 0.01); a visible thyroid enlargement (goiter) with obvious follicular hyperplasia was found in maternal rats; the goiter was not found in their pups, but follicular hyperplasia was observed. (2) The urinary iodine concentrations in those maternal rats of iodine excess groups were significantly paralleled with their iodine intakes of 5, 10, 50, 100 folds; however the iodine content in their milk was only moderately increased, not paralleled with their iodine intake; the pups' urinary iodine was also paralleled with their iodine intake (iodine level in milk). (3) The serum T4 levels in mothers of iodine excess groups were decreased gradually with their increase of iodine intake, but the thyroids were not enlarged; however, some histological changes, manly increased follicles with colloid accumulation and concurrence of follicular hyperplasia, were found in thyroid tissues; especially in 50HI and 100HI groups, the hyperplasia became remarkable. The serum T4 levels in pups of iodine excess groups did not change remarkably with increased iodine intake and hypothyroidism was not found; moderate follicular hyperplasia was only found in 100HI group. Conclusions Excessive iodine can be excreted by urine both in maternal rats and pups after high iodine intake. The lactating mothers with high iodine intake decrease the iodine intake in their offspring via the adjustment of mammary gland. Maternal rats with a long term of iodine excess intake appear hypothyroidism while the thyroid function of their pups in lactation is basically normal. Our findings strongly indicate that parent generation could protect their progeny from the iodine excess in some degree.