Role of Sertoli and Leydig Cells in the Regulation of Spermatogonial Stem Cell and Development of Reproductive Disorders in Male C57Bl/6 Mice with Type 1 Diabetes Mellitus
Role of Sertoli and Leydig Cells in the Regulation of Spermatogonial Stem Cell and Development of Reproductive Disorders in Male C57Bl/6 Mice with Type 1 Diabetes Mellitus
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DOI：
10.1007/s10517-017-3940-6
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发表时间：
2017-11
影响因子：
0.7
通讯作者：
E. Skurikhin;A. Pakhomova;O. Pershina;V. A. Krupin;N. N. Ermakova-N.;E. Pan;A. I. Kudryashova;L. A. Ermolaeva;E. S. Khmelevskaya;V. E. Goldberg;V. Zhdanov;A. Dygai
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文献类型：
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作者：
E. Skurikhin;A. Pakhomova;O. Pershina;V. A. Krupin;N. N. Ermakova-N.;E. Pan;A. I. Kudryashova;L. A. Ermolaeva;E. S. Khmelevskaya;V. E. Goldberg;V. Zhdanov;A. Dygai
对雄性 C57Bl/6 小鼠进行链脲佐菌素治疗会诱发一系列 1 型糖尿病的典型症状：高血糖和胰岛素缺乏、胰腺局灶性炎症浸润、朗格汉斯胰岛的破坏性变化、岛体损伤（PDX1+细胞数量减少和分泌细胞的胰岛素表达减少）。男性生殖障碍是1型糖尿病的严重并发症。在“糖尿病”小鼠中，观察到睾丸组织出现间质水肿伴炎症浸润和微血管紊乱，内皮前体细胞（CD45-/CD31+）的数量以及活动精子的总数和百分比减少，未成熟的生精上皮细胞脱落进入小管管腔。糖尿病中各种精原干细胞群（c-kit-/CD90+、c-kit+/CD90+ 和 CD51-/CD24+/CD52+）增殖和分化的紊乱可以通过炎症因子对产生睾酮的 Leydig 细胞的抑制影响来解释。
Course administration streptozotocin to male C57Bl/6 mice induces a complex of symptoms typical of type 1 diabetes mellitus: hyperglycemia and insulin deficiency, focal inflammatory infiltration of the pancreas, destructive changes in the Langerhans islets, damage to the insular apparatus (reduced number of PDX1+cells and insulin expression by the secreting cells). Male reproductive disorder are serious complications of type 1 diabetes mellitus. In “diabetic” mice, interstitial edema with inflammatory infiltration and microvascular disorders in the testicular tissue are observed, the number of endothelial precursors (CD45—/CD31+) and the total number and percentage of motile spermatozoa decreased, immature spermatogenic epithelium cells are desquamated of into the lumen of the tubules. Disturbances in the proliferation and differentiation of various spermatogonial stem cell populations (c-kit—/CD90+, c-kit+/CD90+, and CD51—/CD24+/CD52+) in diabetes can be explained by the inhibitory influence of inflammatory factors on testosterone-producing Leydig cells.