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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

Authors
  • Skurikhin, E. G.
  • Pakhomova, A. V.
  • Pershina, O. V.
  • Krupin, V. A.
  • Ermakova, N. N.
  • Pan, E. S.
  • Kudryashova, A. I.
  • Ermolaeva, L. A.
  • Khmelevskaya, E. S.
  • Goldberg, V. E.
  • Zhdanov, V. V.
  • Dygai, A. M.
Type
Published Article
Journal
Bulletin of Experimental Biology and Medicine
Publisher
Springer US
Publication Date
Nov 27, 2017
Volume
164
Issue
2
Pages
127–131
Identifiers
DOI: 10.1007/s10517-017-3940-6
Source
Springer Nature
Keywords
License
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Abstract

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.

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