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Raised leptin levels induce oxidative stress, which negatively impacts male reproduction. Profortil® is an antioxidant formulation clinically used to improve sperm quality. Whether Profortil® supplementation can prevent the detrimental effects of leptin on spermatozoa is not known. Thus, the aim of this study was to examine the effects of Profortil® on leptin-induced adverse effects on rat spermatozoa. Adult Sprague-Dawley rats were given either normal saline (control), leptin (60 µg/kg/day), Profortil® (50 mg/kg/day), or Profortil® + leptin once daily for 2 weeks. Sperm count and abnormal morphology were recorded. Testicular levels of 8-hydroxy-2-deoxyguanosine (8-OHdG), superoxide dismutase (SOD), and catalase (CAT) activities were measured. TUNEL and Comet assays were performed. The sperm count in the Profortil® + leptin group was comparable to that in controls but was significantly higher than that in the leptin group, which was significantly lower than that in controls. Sperm morphology was not different between leptin and Profortil® + leptin groups. 8-OHdG level was significantly lower in the Profortil® + leptin group than that in the leptin group but was comparable to that in controls. CAT activity was not different between leptin and Profortil® + leptin groups, although activity in the former was significantly lower than that in controls. SOD activity was not different between groups. The apoptotic index was significantly higher in the leptin and Profortil® + leptin groups than in the control and Profortil® groups. Sperm DNA fragmentation was not significantly different between leptin and Profortil® + leptin groups. In conclusion, Profortil®, when given at 50 mg/kg/day for 3 weeks, was only able to reduce some, but not all the adverse effects of leptin on sperm parameters. [ABSTRACT FROM AUTHOR]

Introduction Obesity increases risks of male infertility, but bariatric surgery does not improve semen quality. Recent uncontrolled studies suggest that a low-energy diet (LED) improves semen quality. Further evaluation within a randomized, controlled setting is warranted. Methods Men with obesity (18-60 years) with normal sperm concentration (normal count) (n = 24) or oligozoospermia (n = 43) were randomized 1:1 to either 800 kcal/day LED for 16 weeks or control, brief dietary intervention (BDI) with 16 weeks' observation. Semen parameters were compared at baseline and 16 weeks. Results Mean age of men with normal count was 39.4 ± 6.4 in BDI and 40.2 ± 9.6 years in the LED group. Mean age of men with oligozoospermia was 39.5 ± 7.5 in BDI and 37.7 ± 6.6 years in the LED group. LED caused more weight loss than BDI in men with normal count (14.4 vs 6.3 kg; P <.001) and men with oligozoospermia (17.6 vs 1.8 kg; P <.001). Compared with baseline, in men with normal count total motility (TM) increased 48 ± 17% to 60 ± 10% (P <.05) after LED, and 52 ± 8% to 61 ± 6% (P <.0001) after BDI; progressive motility (PM) increased 41 ± 16% to 53 ± 10% (P <.05) after LED, and 45 ± 8% to 54 ± 65% (P <.001) after BDI. In men with oligozoospermia compared with baseline, TM increased 35% [26] to 52% [16] (P <.05) after LED, and 43% [28] to 50% [23] (P =.0587) after BDI; PM increased 29% [23] to 46% [18] (P <.05) after LED, and 33% [25] to 44% [25] (P <.05) after BDI. No differences in postintervention TM or PM were observed between LED and BDI groups in men with normal count or oligozoospermia. Conclusion LED or BDI may be sufficient to improve sperm motility in men with obesity. The effects of paternal dietary intervention on fertility outcomes requires investigation. [ABSTRACT FROM AUTHOR]