Department of Biotechnology, All India Institute of Medical Sciences, New Delhi, 110029, India.
Reprod Sci. 2023 Nov;30(11):3339-3352. doi: 10.1007/s43032-023-01278-w. Epub 2023 Jun 15.
Male reproductive functions and bone health are both adversely affected by the high salt diet (HSD). Nevertheless, the underlying mechanism via which it alters the sperm function remains largely unknown. This study examines the mechanism by which HSD affects male fertility by impairing bone health. For investigating the same, male BALB/c mice were categorized into three groups-HSD group (fed with 4% NaCl), a low salt diet (LSD) group (fed with 0.4% NaCl), and a control group (fed with a normal diet) for 6 weeks and thereafter assessed for various sperm parameters, bone turnover markers, and testosterone levels. Furthermore, the quantitative assessment of testosterone biosynthesis enzymes was performed. Interestingly, we observed that mice fed with HSD showed significant alterations in sperm parameters-motility, count, and vitality, including morphological changes compared to both the LSD and the control groups. In addition, serum analysis showed an increase in bone resorption markers and a decrease in bone formation markers in the HSD group (p < 0.05). Further, HSD caused a decrease in the testosterone level and mRNA expression of testosterone biosynthesis enzymes. Importantly, a significant decrease in bone formation marker osteocalcin (OC) was observed to coincide with the dip in testosterone level in the HSD group. Given that OC plays a key role in maintaining male fertility, the above findings suggest that a decrease in OC levels may affect the testosterone biosynthesis pathway, reducing testosterone hormone secretion and thereby resulting in decreased spermatogenesis. The study for the first time delineates and bridges the mechanism of HSD-mediated bone loss (results in a deficiency of OC) with decreased testosterone biosynthesis and thus impaired male fertility.
高盐饮食（HSD）会对男性生殖功能和骨骼健康产生不利影响。然而，其改变精子功能的潜在机制在很大程度上仍不清楚。本研究通过损害骨骼健康来研究 HSD 如何影响男性生育能力的机制。为此，将雄性 BALB/c 小鼠分为三组-HSD 组（喂食 4%NaCl）、低盐饮食（LSD）组（喂食 0.4%NaCl）和对照组（喂食正常饮食），持续 6 周，然后评估各种精子参数、骨转换标志物和睾酮水平。此外，还进行了睾酮生物合成酶的定量评估。有趣的是，我们观察到喂食 HSD 的小鼠的精子参数（活力、计数和活力）发生了显著变化，与 LSD 和对照组相比，精子形态也发生了变化。此外，血清分析显示 HSD 组的骨吸收标志物增加，骨形成标志物减少（p<0.05）。此外，HSD 导致睾酮水平和睾酮生物合成酶的 mRNA 表达降低。重要的是，在 HSD 组中观察到骨形成标志物骨钙素（OC）的显著下降与睾酮水平的下降相吻合。鉴于 OC 在维持男性生育能力方面发挥着关键作用，上述发现表明 OC 水平的降低可能会影响睾酮生物合成途径，减少睾酮激素的分泌，从而导致精子发生减少。该研究首次阐明并桥接了 HSD 介导的骨丢失（导致 OC 缺乏）与降低的睾酮生物合成之间的机制，从而导致男性生育能力受损。
