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Abstract

Because diabetes mellitus (DM) poses harm to the reproductive systems of humans and mice on both the cellular and histological levels, we sought to understand the effects of streptozotocin-induced (STZ) diabetes mellitus on the spermatogenesis and Anti-Müllerian hormone (AMH) production of mice. The structural integrity of the testes is disrupted due to the high levels of oxidative stress caused by DM, which also hinders spermatogenesis. Advanced glycation end products (AGEs) have been found to induce autophagy in Sertoli cells, and the Sertoli cells of diabetic models have fewer tight junctions between them. This disorganization and decreased integrity of the seminiferous tubules negatively impact sperm viability. Sperm motility and survival rates are reduced due to decreased cellular respiration and damage to DNA integrity. The testes of eight C57/BL6J mice (four control, four diabetic, euthanized at fourteen weeks) were analyzed using immunohistochemistry and light microscopy. IHC staining revealed that AMH production by Sertoli cells was decreased and, in diabetic mice, was secreted mainly in the basal region of the seminiferous tubules. Additionally, the sperm count revealed that control mice had 90±1.97 sperm per seminiferous tubule section, while diabetic seminiferous tubule sections contained 27±8.31 sperm. Comparison of the control and diabetic sperm counts using a t-test provided a P value of .013. Finally, examination of the seminiferous tubule sections revealed that the control mice had a more organized tubule structure and circular lumen compared to the disorganized and irregular seminiferous tubules of the diabetic mice. To further study this research question, sperm viability could be analyzed by examining the mitochondrial accumulation and activity of spermatozoa in diabetic mice.

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