Introduction: Diabetes mellitus (DM) may cause male infertility acting with pre-testicular, testicular and post-testicular mechanism.
Aim: To evaluate the presence of male infertility and the mechanisms of sperm damage in diabetic patients in childbearing age.
Patients and methods: Thirty-four patients with DM1, 55 with DM2 and 100 healthy fertile men (controls) were enrolled. Diabetic patients were further divided into three groups based on their glycometabolic status and illness duration. Conventional and biofunctional sperm parameters were evaluated by standard semen analysis and flow cytometry. This latter included sperm DNA fragmentation, vitality, early and late apoptosis, chromatin condensation, mitochondrial membrane potential (MMP), leukocyte subpopulations, lipid peroxidation (PL) and sperm mitochondrial superoxide. In addition, all patients and controls underwent testicular ultrasound sca and serum LH and testosterone measurements.
Results: Diabetic patients had lower sperm concentration, progressive motility and morphology vs controls (P<0.05). The ejaculate volume is significantly lower in patients with DM1 vs controls (P<0.05). Leukocyte concentrations were higher in patients with DM2 (P<0.05), showing a statistically significant reduction in the percentage of T helper cells and an increase of the suppressor T lymphocytes compared to controls (P<0.05). The analysis of the biofunctional sperm parameters showed worsening MMP in diabetic patients (P<0.05). Patients with DM2 showed a significant decrease in the degree of sperm vitality and increased spermatozoa in late apoptosis vs Controls and of the DNA fragmentation compared to the other two groups (P<0.05). Moreover, patients with DM1 had a lower progressive motility when the disease duration was >10 years vs the other two groups, and lower MMP after 5 years of disease (P<0.05). The degree of PL was higher in DM2 patients compared to the other two groups (P<0.05), while the concentrations of mitochondrial superoxide were greater in DM2 patients compared to DM1 and control group (P<0.05). The ultrasound data showed that the diameter of the epididymal head and tail after ejaculation were greater in patients with DM1 long term than those of short duration compared to controls (P<0.05). Testosterone levels were lower in DM2 patients vs controls (P<0.05).
Conclusion: Patients with DM1 have low ejaculate volume for an altered epididymal emptying and a mitochondrial damage that anticipates the later decline of sperm motility. DM2 is instead characterized by an inflammatory condition with increased leukocyte and oxidative stress and elevated levels of sperm DNA fragmentation and decreased sperm vitality.
20 - 23 May 2017
European Society of Endocrinology