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<p>Male obesity-related secondary hypogonadism (MASH), also referred to as metabolic hypogonadism, is an increasingly recognised clinical condition of growing relevance, with significant implications for reproductive, metabolic, and cardiovascular health. Excess adipose tissue, particularly with visceral distribution, impairs the function of the hypothalamic-pituitary-gonadal axis through complex endocrine mechanism. These include alterations in leptin and insulin levels, the development of chronic low-grade inflammation, and reduced levels of sex hormone-binding globulin, ultimately leading to decreased total and free testosterone levels. This condition is frequently associated with insulin resistance, metabolic syndrome, and increased cardiovascular risk, thereby establishing a vicious cycle that further exacerbates metabolic morbidity. Diagnosis requires a careful clinical evaluation supported by repeated serum total testosterone measurements interpreted within the context of the patient’s overall metabolic profile. Management primarily based on targeted lifestyle interventions, whereas testosterone replacement therapy should be reserved for selected cases, following a thorough assessment of the risks-benefit ratio. This review summarises the current evidence on the pathophysiology, diagnosis, and management of metabolic hypogonadism, and proposes a multidisciplinary approach aimed at reducing metabolic and cardiovascular risk.</p>

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Ipogonadismo metabolico maschile: una forma di ipogonadismo funzionale nell’uomo obeso

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月17日

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  • Luca Guadagnino,
  • Rossella Cannarella,
  • Aldo E. Calogero

摘要

Male obesity-related secondary hypogonadism (MASH), also referred to as metabolic hypogonadism, is an increasingly recognised clinical condition of growing relevance, with significant implications for reproductive, metabolic, and cardiovascular health. Excess adipose tissue, particularly with visceral distribution, impairs the function of the hypothalamic-pituitary-gonadal axis through complex endocrine mechanism. These include alterations in leptin and insulin levels, the development of chronic low-grade inflammation, and reduced levels of sex hormone-binding globulin, ultimately leading to decreased total and free testosterone levels. This condition is frequently associated with insulin resistance, metabolic syndrome, and increased cardiovascular risk, thereby establishing a vicious cycle that further exacerbates metabolic morbidity. Diagnosis requires a careful clinical evaluation supported by repeated serum total testosterone measurements interpreted within the context of the patient’s overall metabolic profile. Management primarily based on targeted lifestyle interventions, whereas testosterone replacement therapy should be reserved for selected cases, following a thorough assessment of the risks-benefit ratio. This review summarises the current evidence on the pathophysiology, diagnosis, and management of metabolic hypogonadism, and proposes a multidisciplinary approach aimed at reducing metabolic and cardiovascular risk.