BACKGROUND Diabetes and hypothyroidism produce adverse effects on body weight and sexual maturity by inhibiting body growth and metabolism. The occurrence of diabetes is always accompanied with thyroid dysfunction. Thus, it is important to take hypo- or hyper-thyroidism into consideration when exploring the adverse effects caused by diabetes. Previous reports have found hypothyroidism inhibits testicular growth by delaying Sertoli cell differentiation and proliferation. Hence, by establishing a mouse model of diabetes combined with hypothyroidism, we provided evidence that poly glandular autoimmune syndrome affected testicular development and spermatogenesis. RESULTS we mimicked polyglandular deficiency syndrome in both immature and prepubertal mice by induction of diabetes and hypothyroidism, which caused decreases in serum concentrations of testosterone and insulin like growth factor 1 (IGF-1). Such reduction of growth factor resulted in inhibition of testicular and epididymal development. Moreover, expressions of Claudin-11 were observed between Sertoli cells and disrupted in the testes of syndrome group mice. We also found reduced sperm count and motility in prepubertal mice. CONCLUSIONS This mimicry of the diabetes and thyroid dysfunction, will be helpful to better understand the reasons for male infertility in diabetic-cum-hypothyroid patients.

中文翻译：

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糖尿病和甲状腺功能减退症同时对小鼠生精小管内Claudin-11的生精和免疫定位的影响。

背景技术糖尿病和甲状腺功能减退症通过抑制身体的生长和代谢而对体重和性成熟产生不利影响。糖尿病的发生总是伴随着甲状腺功能障碍。因此，在探究糖尿病引起的不良反应时，必须考虑甲状腺功能低下或甲状腺功能亢进。先前的报道发现甲状腺功能减退症通过延迟Sertoli细胞的分化和增殖来抑制睾丸生长。因此，通过建立糖尿病合并甲状腺功能减退症的小鼠模型，我们提供了多腺体自身免疫综合症影响睾丸发育和精子发生的证据。结果我们通过诱导糖尿病和甲状腺功能减退来模仿未成熟和青春期前小鼠的多腺缺陷综合征，这会导致血清睾丸激素和胰岛素样生长因子1（IGF-1）的浓度降低。生长因子的这种减少导致睾丸和附睾发育的抑制。此外，在支持细胞之间观察到Claudin-11的表达，并且在综合征组小鼠的睾丸中破坏了Claudin-11的表达。我们还发现青春期前小鼠的精子数量和活力降低。结论这种对糖尿病和甲状腺功能障碍的模仿将有助于更好地了解糖尿病合并甲状腺功能减退患者的男性不育原因。我们还发现青春期前小鼠的精子数量和活力降低。结论这种对糖尿病和甲状腺功能障碍的模仿将有助于更好地了解糖尿病合并甲状腺功能减退患者的男性不育原因。我们还发现青春期前小鼠的精子数量和活力降低。结论这种对糖尿病和甲状腺功能障碍的模仿将有助于更好地了解糖尿病合并甲状腺功能减退患者的男性不育原因。