Journal of reproductive immunology · 2026
Puerarin ameliorates obesity-induced spermatogenic dysfunction by restoring Sertoli cell glycolytic homeostasis.
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Wang Xianghong, Ma Duo, Jiang Jing, Wu Shikui, Wu Xian
Аннотация
BACKGROUND: Obesity induced by a high-fat diet (HFD) is closely associated with male infertility. It impairs spermatogenesis and reduces sperm quality. Puerarin (PU), a major isoflavone derived from Pueraria lobata, shows anti-inflammatory, antioxidant, and metabolic regulatory activities. However, its role in obesity-associated spermatogenic dysfunction remains unclear, especially in relation to Sertoli cell glycolytic metabolism.
OBJECTIVES: This study aimed to determine whether PU protects against HFD-induced spermatogenic dysfunction and to examine the involvement of Sertoli cell function and glycolytic homeostasis.
MATERIALS AND METHODS: Male C57BL/6 J mice were fed a normal diet or HFD for 12 weeks. HFD-fed mice then received PU (100 mg/kg/day) or vehicle by oral gavage for 8 weeks. Body weight, glucose tolerance, reproductive tissue histology, sperm parameters, apoptosis-related markers, Sertoli cell markers, and glycolysis-related enzymes were examined. TM4 Sertoli cells were exposed to palmitic acid (PA) to mimic lipotoxic injury and then treated with PU. Cell viability, apoptosis-related genes, lactate and pyruvate production, glycolysis-related proteins, glucose uptake, ATP production, and the effect of glycolytic blockade with 2-DG were assessed. All cell experiments were independently repeated at least three times.
RESULTS: PU attenuated HFD-induced weight gain and improved glucose intolerance. It also improved testicular and epididymal histology, increased sperm count, and reduced sperm abnormalities. In HFD-fed mice, PU increased the Bcl-2/Bax ratio, restored the expression of Sertoli cell-associated markers, including vimentin, WT1, and GATA4, and elevated the expression of HK2, PKM2, and LDHA in the testes. In PA-treated TM4 cells, PU improved cell viability, corrected lactate/pyruvate-related metabolic disturbance, and restored glycolysis-related protein expression.
DISCUSSION: These findings suggest that puerarin protects against HFD-induced spermatogenic impairment by improving metabolic disorders, preserving testicular structure, reducing germ cell apoptosis, and restoring Sertoli cell function. The enhancement of glycolytic metabolism in Sertoli cells may represent an important mechanism by which puerarin supports spermatogenesis under obese conditions.
CONCLUSION: PU alleviated HFD-induced spermatogenic dysfunction. Its protective effects were associated with reduced testicular apoptosis and restoration of Sertoli cell-related glycolytic homeostasis. These findings support PU as a potential therapeutic candidate for obesity-associated male reproductive dysfunction.
OBJECTIVES: This study aimed to determine whether PU protects against HFD-induced spermatogenic dysfunction and to examine the involvement of Sertoli cell function and glycolytic homeostasis.
MATERIALS AND METHODS: Male C57BL/6 J mice were fed a normal diet or HFD for 12 weeks. HFD-fed mice then received PU (100 mg/kg/day) or vehicle by oral gavage for 8 weeks. Body weight, glucose tolerance, reproductive tissue histology, sperm parameters, apoptosis-related markers, Sertoli cell markers, and glycolysis-related enzymes were examined. TM4 Sertoli cells were exposed to palmitic acid (PA) to mimic lipotoxic injury and then treated with PU. Cell viability, apoptosis-related genes, lactate and pyruvate production, glycolysis-related proteins, glucose uptake, ATP production, and the effect of glycolytic blockade with 2-DG were assessed. All cell experiments were independently repeated at least three times.
RESULTS: PU attenuated HFD-induced weight gain and improved glucose intolerance. It also improved testicular and epididymal histology, increased sperm count, and reduced sperm abnormalities. In HFD-fed mice, PU increased the Bcl-2/Bax ratio, restored the expression of Sertoli cell-associated markers, including vimentin, WT1, and GATA4, and elevated the expression of HK2, PKM2, and LDHA in the testes. In PA-treated TM4 cells, PU improved cell viability, corrected lactate/pyruvate-related metabolic disturbance, and restored glycolysis-related protein expression.
DISCUSSION: These findings suggest that puerarin protects against HFD-induced spermatogenic impairment by improving metabolic disorders, preserving testicular structure, reducing germ cell apoptosis, and restoring Sertoli cell function. The enhancement of glycolytic metabolism in Sertoli cells may represent an important mechanism by which puerarin supports spermatogenesis under obese conditions.
CONCLUSION: PU alleviated HFD-induced spermatogenic dysfunction. Its protective effects were associated with reduced testicular apoptosis and restoration of Sertoli cell-related glycolytic homeostasis. These findings support PU as a potential therapeutic candidate for obesity-associated male reproductive dysfunction.