Ruiz-Valderrama Lorena, Mendoza-Sánchez José Edwin, Rodríguez-Tobón Ernesto, Arrieta-Cruz Isabel, González-Márquez Humberto, Salame-Méndez Pablo Arturo, Tarragó-Castellanos Rosario, Cortés-Barberena Edith, Rodríguez-Tobón Ahiezer, Arenas-Ríos Edith
Departamento de Biología de la Reproducción, Universidad Autónoma Metropolitana, Iztapalapa, Ciudad de México 09340, Mexico.
Doctorado en Biología Experimental, Universidad Autónoma Metropolitana, Iztapalapa, Ciudad de México 09340, Mexico.
Int J Mol Sci. 2025 Feb 21;26(5):1850. doi: 10.3390/ijms26051850.
Infertility is increasingly recognized as being closely linked to obesity in humans. The successful production of fertile spermatozoa requires adequate spermatogenesis within the testis and proper spermatozoa maturation through the epididymis. This study aimed to evaluate the impact of body adiposity on male fertility, focusing on sperm parameters, epididymal sperm maturation, and sperm capacitation in Wistar rats. Male rats were randomized into three dietary groups over four weeks: a control group receiving less than 4% lard, regular chow, a 10% lard group, and a 60% lard group. Following dietary interventions, fertility tests were conducted across the groups. The epididymis was dissected into caput, corpus, and cauda regions to assess sperm concentration, vitality capacitation, carbohydrate distribution, tyrosine phosphorylation, and phosphatidylserine levels. Additionally, serum testosterone levels were measured to evaluate hormonal influences on fertility. The rats subjected to high-fat diets leading to overweight and obesity exhibited significant alterations in fertility. These changes were characterized by impaired epididymal sperm maturation, as evidenced by lower testosterone levels, decreased sperm viability, and capacitation. Furthermore, increased adiposity was associated with a lack of asymmetry in the plasma membrane, alteration in carbohydrate distribution, and changes in tyrosine phosphorylation. This study underscores the adverse effects of high-fat diets on male fertility, particularly through mechanisms affecting sperm maturation in the epididymis. The evidence suggests that obesity-induced alterations in sperm parameters and hormonal profiles may contribute to reduced fertility in male rats, which could have implications for understanding similar human processes.
在人类中，不孕症越来越被认为与肥胖密切相关。成功产生可育精子需要睾丸内有足够的精子发生，以及精子通过附睾进行适当的成熟。本研究旨在评估身体肥胖对雄性生育能力的影响，重点关注Wistar大鼠的精子参数、附睾精子成熟和精子获能。雄性大鼠在四周内被随机分为三个饮食组：对照组接受少于4%的猪油、常规饲料，10%猪油组和60%猪油组。饮食干预后，对各组进行生育力测试。将附睾分为头、体、尾区域，以评估精子浓度、活力、获能、碳水化合物分布、酪氨酸磷酸化和磷脂酰丝氨酸水平。此外，测量血清睾酮水平以评估激素对生育能力的影响。食用导致超重和肥胖的高脂饮食的大鼠在生育能力方面表现出显著变化。这些变化的特征是附睾精子成熟受损，表现为睾酮水平降低、精子活力和获能下降。此外，肥胖增加与质膜缺乏不对称性、碳水化合物分布改变以及酪氨酸磷酸化变化有关。本研究强调了高脂饮食对雄性生育能力的不利影响，特别是通过影响附睾精子成熟的机制。证据表明，肥胖引起的精子参数和激素谱改变可能导致雄性大鼠生育能力下降，这可能对理解类似的人类过程有启示意义。
