The Effect of Immobilization Stress on the Morphofunctional State of Leydig Cells in the Offspring of Female Rats with Experimental Type 1 Diabetes

The aim of study was to analyze the morphofunctional state of Leydig cells of the testes in sexually mature offspring of female rats with experimental type 1 diabetes mellitus exposed to immobilization stress.

Material and methods. The study included sexually mature (70-day) offspring of female rats with experimental type 1 diabetes. To achieve the aim, type 1 diabetes was simulated in experimental animals using streptozotocin. All animals were subjected to immobilization stress using Kogan chambers in order to assess their antistress resistance. The object of the study was the testes of sexually mature offspring from female rats with experimental type 1 diabetes. Serial histological sections were used to determine the area of interstitial tissue and testis parenchyma. The number of Leydig cells, including the fractions of active and inactive endocrinocytes, was calculated; the activity index, a coefficient reflecting the ratio of the total number of Leydig cells to that of Sertoli cells per 1 convoluted tubule, and a coefficient representing the ratio of the number of endocrinocytes to the total number of spermatogenic cells were calculated based on one convoluted seminiferous tubule.

Results. Leydig cells in the offspring of female rats with experimental type 1 diabetes mellitus have a reduced antistress resistance; that is supported by a more pronounced decrease in the number of endocrinocytes and a change in their subpopulation composition: a decrease in the number of active Leydig cells and, conversely, an increase in the number of inactive cells, which, in turn, results in a decrease in the index endocrinocyte activity, and a decrease in blood testosterone levels. As a result, immobilization stress causes inhibition of spermatogenesis in experimental animals.

Conclusion. Simulated type 1 diabetes mellitus in female rats results in the birth of offspring characterized by impaired spermatogenesis; this may be due to violation of the morphofunctional state of Leydig cells, and a decrease in the antistress resistance of testicular endocrinocytes.

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