article · Frontiers in Endocrinology
Stress is known to impair male fertility through oxidative stress, but gonadotropin inhibitory hormone (GnIH) also serves as a central driver in this process. Evidence demonstrates that GnIH triggers the hypothalamic-pituitary-adrenal axis, resulting in elevated corticosteroid release. Simultaneously, GnIH suppresses the hypothalamic-pituitary-thyroidal axis, halting the conversion of thyroxine into triiodothyronine. It also impedes the release of kisspeptin and gonadotropin-releasing hormone, which disrupts the hypothalamic-pituitary-testicular axis and lowers testosterone biosynthesis. Together, these hormonal disruptions alter testicular structure, impair steroid production in both the adrenal glands and testes, reduce sperm generation, and compromise overall sperm quality and performance. Because GnIH exerts these extensive negative effects across multiple pathways, inhibiting its activity during periods of stress presents a viable therapeutic or preventative strategy for protecting male fertility.
Psychological and physiological stress can severely disrupt male reproductive health. By detailing how gonadotropin inhibitory hormone orchestrates multiple hormonal pathways to reduce sperm quality and testosterone production, this insight clarifies the biological links between stress and infertility. Understanding these mechanisms helps researchers identify precise physiological targets to mitigate or prevent reproductive impairment caused by chronic stress.
This work identifies gonadotropin inhibitory hormone as an early-stage target for therapeutic or prophylactic interventions aimed at stress-related male infertility. Pharmaceutical developers could potentially design GnIH-suppressing drugs to protect sperm quality and hormonal balance under stress. However, as the findings represent a review of biological mechanisms, any commercial application remains at an early conceptual stage, requiring dedicated drug development and clinical validation.
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Studies have implicated oxidative stress-sensitive signaling in the pathogenesis of stress-induced male infertility. However, apart from oxidative stress, gonadotropin inhibitory hormone (GnIH) plays a major role. The present study provides a detailed review of the role of GnIH in stress-induced male infertility. Available evidence-based data revealed that GnIH enhances the release of corticosteroids by activating the hypothalamic-pituitary-adrenal axis. GnIH also mediates the inhibition of the conversion of thyroxine (T4) to triiodothyronine (T3) by suppressing the hypothalamic-pituitary-thyroidal axis. In addition, GnIH inhibits gonadotropin-releasing hormone (GnRH), thus suppressing the hypothalamic-pituitary-testicular axis, and by extension testosterone biosynthesis. More so, GnIH inhibits kisspeptin release. These events distort testicular histoarchitecture, impair testicular and adrenal steroidogenesis, lower spermatogenesis, and deteriorate sperm quality and function. In conclusion, GnIH, via multiple mechanisms, plays a key role in stress-induced male infertility. Suppression of GnIH under stressful conditions may thus be a beneficial prophylactic and/or therapeutic strategy.
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DOI: 10.3389/fendo.2023.1329564
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