Unraveling the impact of semaglutide in a diabetic rat model of testicular dysfunction: Insights into spermatogenesis pathways and miRNA-148a-5p.

BACKGROUND

Diabetes has been a long-known risk factor for male sexual dysfunction, which may be caused by persistent hyperglycemia, oxidative stress, and spermatogenesis inhibition. This study explored the potential of Semaglutide (Sem) to alleviate testicular dysfunction and spermatogenesis impairment in diabetic rats to understand the molecular mechanism of this protective effect.

METHODOLOGY: A controlled experiment was conducted where 28 adult male rats were divided into four groups: control, Semaglutide, diabetic, and diabetes + Sem. Diabetes was induced using a single STZ dose (50 mg/kg, i.p.). At the same time, Sem was administered as a daily subcutaneous dose (25 nmol/kg) for four weeks after the confirmed diagnosis of diabetes. Several biochemical and histochemical analyses were performed in addition to mating behavior assessments. The estimation of spermatogenesis-related genes and proteins was conducted using PCR and western blotting techniques.

RESULTS

revealed promising outcomes, wherein Sem treatment effectively mitigated diabetes-induced sexual and testicular dysfunction. Specifically, it regulated the disrupted redox balance, restored spermatogenesis gene and protein levels, modulated hormonal profiles, and mitigated testicular inflammation.

CONCLUSION

Sem protects against diabetes-induced testicular and sexual impairments by influencing several pathways and restoring spermatogenesis-related genes and proteins. Future studies may involve a potential investigation of Sem translational applications in clinical settings for treating male infertility associated with diabetes.