Division of Life Science, Graduate School of Science and Engineering, Saitama University, Saitama 338-8570, Japan,
National Institute of Occupational Safety and Health, Kawasaki 214-8585, Japan.
Zoolog Sci. 2021 Jun;38(3):238-246. doi: 10.2108/zs200063.
Growth-retarded () mice display primary congenital hypothyroidism due to the hyporesponsiveness of their thyroid glands to thyroid-stimulating hormone (TSH). We examined somatic growth, anterior pituitary development, and hormonal profiles in female mice and normal ones. Although growth in females was suppressed 2 weeks after birth, the measured growth parameters and organ weights gradually increased and finally reached close to the normal levels. mice exhibited delayed eye and vaginal openings and remained in a state of persistent diestrus thereafter, plasma estrogen levels being lower than those in normal mice. mice that received normal-donor thyroids showed accelerated growth and their body weights increased up to the sham-normal levels, indicating the importance of early thyroid hormone supplementation. In the anterior pituitary, there were fewer growth hormone (GH) and prolactin (PRL) cells in mice than in normal mice as examined at 12 weeks after birth, but the numbers of these cells did not differ from those in normal mice after 24 weeks. mice had more TSH cells than normal mice until 48 weeks. Plasma GH levels in mice were lower than those in normal mice at 2 weeks, but did not differ substantially after 5 weeks. Compared with normal mice, mice had significantly lower plasma PRL and thyroxine levels, but notably higher TSH levels until 48 weeks. These findings indicate that thyroid hormone deficiency in mice causes delayed development and growth, and inappropriate development of GH, PRL and TSH cells, followed by the abnormal secretion of hormones by these pituitary cells.
生长迟缓（）的小鼠由于甲状腺对促甲状腺激素（TSH）的反应性降低而表现出原发性先天性甲状腺功能减退症。我们检查了雌性和正常的生长迟缓（）小鼠的体生长、前垂体发育和激素谱。尽管生长迟缓（）的雌性小鼠在出生后 2 周内生长受到抑制，但测量的生长参数和器官重量逐渐增加，最终接近正常水平。生长迟缓（）的小鼠表现出眼睛和阴道开口延迟，并在此后一直处于持续发情期，其血浆雌激素水平低于正常小鼠。接受正常供体甲状腺的生长迟缓（）小鼠表现出加速生长，体重增加至接近假正常水平，表明早期补充甲状腺激素的重要性。在前垂体中，与正常小鼠相比，出生后 12 周时生长迟缓（）的小鼠中的生长激素（GH）和催乳素（PRL）细胞较少，但 24 周后这些细胞的数量与正常小鼠没有差异。生长迟缓（）的小鼠比正常小鼠有更多的 TSH 细胞，直到 48 周。生长迟缓（）的小鼠在 2 周时的血浆 GH 水平低于正常小鼠，但 5 周后差异不大。与正常小鼠相比，生长迟缓（）的小鼠的血浆 PRL 和甲状腺素水平明显较低，但直到 48 周时 TSH 水平明显较高。这些发现表明，甲状腺激素缺乏导致生长迟缓（）小鼠发育和生长延迟，以及 GH、PRL 和 TSH 细胞发育不当，随后这些垂体细胞分泌激素异常。
