Insights from a Study on NMN's role in Increasing sperm count

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- Updated by Jody Mullis
Medically reviewed by Dr. Sidra Samad

Nicotinamide mononucleotide improves spermatogenic function in streptozotocin-induced diabetic mice via modulating the glycolysis pathway


Published in "Acta Biochim Biophys Sin" in 2022, this study focuses on the impact of nicotinamide mononucleotide (NMN) on testicular spermatogonia function in mice that have been injected with streptozotocin (STZ), a chemical that induces type 1 diabetes, which often leads to spermatogonia dysfunction. The researchers aim to provide a better understanding and potential treatment for the reduction in fertility associated with diabetes. The study can be found here.

The study found that when NMN was orally administered to STZ-induced diabetic mice, there was a significant increase in both body and testis weight and sperm count. Furthermore, it was observed that NMN treatment led to a significant reduction in the number of abnormal sperm and the rate of sperm malformation.

Analysis of histological data showed that NMN treatment significantly increased the area and diameter of seminiferous tubules, which are structures within the testes where sperm is produced. Additionally, it was found that NMN increased the number of spermatogenic cells (cells involved in the production of sperm) and sperm.

The researchers also examined NMN's impact on the expressions of Bcl-2 and Bax, two proteins that play a critical role in cell apoptosis or programmed cell death, in the testis. The results showed that NMN increased the expression of Bcl-2, which inhibits apoptosis, and decreased the expression of Bax, promoting apoptosis.

Moreover, the study found that NMN increased the protein expression of Vimentin and the mRNA expressions of WT1 and GATA4, which are important for cell structure and gene regulation.

NMN also enhanced the expressions of glycolysis-related rate-limiting enzymes including HK2, PKM2, and LDHA. Glycolysis is the metabolic pathway that converts glucose into pyruvate, producing ATP, the energy that powers cells.

In conclusion, NMN demonstrated protective effects on the testis, specifically improving spermatogenic function in STZ-induced diabetic mice. It achieves this protective effect by reducing spermatogenic cell apoptosis through the regulation of glycolysis in Sertoli cells, cells that support and nourish the spermatogenic cells in the testis. These findings provide significant implications for the future clinical application of NMN in the treatment of diabetes-induced spermatogenic dysfunction.

Key takeaways:

  • NMN enhances testicular spermatogenic function in STZ-induced diabetic mice.
  • NMN treatment increases body, testis weight, and sperm count, and reduces the number of abnormal sperm and sperm malformation rate.
  • NMN increases the size of seminiferous tubules and the number of spermatogenic cells and sperm.
  • NMN affects apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax.
  • NMN impacts gene regulation and expression of crucial proteins, including Vimentin, WT1, and GATA4.
  • NMN plays a role in energy production by increasing the expressions of glycolysis-related rate-limiting enzymes including HK2, PKM2, and LDHA.