Moreira Ruben J, Oliveira Pedro F, Spadella Maria Angélica, Ferreira Rita, Alves Marco G
Institute of Biomedicine, Department of Medical Sciences (iBiMED), University of Aveiro, 3810-193 Aveiro, Portugal.
LAQV-REQUIMTE, Department of Chemistry, University of Aveiro, 3810-193 Aveiro, Portugal.
Antioxidants (Basel). 2025 Jan 27;14(2):150. doi: 10.3390/antiox14020150.
Obesity results from a disproportionate accumulation of fat and has become a global health concern. The increase in adipose tissue is responsible for several systemic and testicular changes including hormone levels (leptin, adiponectin, testosterone, estrogen), inflammatory cytokines (increase in TNF-α and IL-6 and decrease in IL-10), and redox state (increase in reactive oxygen species and reduction in antioxidant enzymes). This results in poor sperm quality and compromised fertility in men with obesity. Lifestyle modifications, particularly diet transition to caloric restriction and physical exercise, are reported to reverse these negative effects. Nevertheless, precise mechanisms mediating these benefits, including how they modulate testicular oxidative stress, inflammation, and metabolism, remain to be fully elucidated. The main pathway described by which these lifestyle interventions reverse obesity-induced oxidative damage is the Nrf2-SIRT1 axis, which modulates the overexpression of antioxidant defenses. Of note, some of the detrimental effects of obesity on the testis are inherited by the descendants of individuals with obesity, and while caloric restriction reverses some of these effects, no significant work has been carried out regarding physical exercise. This review discusses the consequences of obesity-induced testicular oxidative stress on adult and pediatric populations, emphasizing the therapeutic potential of lifestyle to mitigate these detrimental effects.
肥胖是由于脂肪过度堆积所致，已成为全球关注的健康问题。脂肪组织的增加会引发多种全身和睾丸变化，包括激素水平（瘦素、脂联素、睾酮、雌激素）、炎性细胞因子（肿瘤坏死因子-α和白细胞介素-6增加，白细胞介素-10减少）以及氧化还原状态（活性氧增加，抗氧化酶减少）。这会导致肥胖男性精子质量差和生育能力受损。据报道，生活方式的改变，尤其是向热量限制饮食和体育锻炼的转变，可逆转这些负面影响。然而，介导这些益处的精确机制，包括它们如何调节睾丸氧化应激、炎症和代谢，仍有待充分阐明。这些生活方式干预措施逆转肥胖诱导的氧化损伤所描述的主要途径是Nrf2-SIRT1轴，它调节抗氧化防御的过度表达。值得注意的是，肥胖对睾丸的一些有害影响会由肥胖个体的后代遗传，虽然热量限制可逆转其中一些影响，但关于体育锻炼尚未开展重要研究。本综述讨论了肥胖诱导的睾丸氧化应激对成人和儿童人群的影响，强调了生活方式减轻这些有害影响的治疗潜力。
