Roles of gas molecules and related factors in knee cartilage injury and repair: a bibliometric visualization analysis of research hotspots.

Male obesity secondary hypogonadism (MOSH), also termed functional hypogonadism, represents one of the most prevalent endocrine disorders among men with excess adiposity [,]. Epidemiological data consistently demonstrate an inverse relationship between body mass index (BMI) and serum testosterone concentrations, with obese men exhibiting total testosterone levels 25–30% lower than their lean counterparts [,]. The clinical consequences of this hormonal deficit extend beyond reproductive dysfunction and encompass metabolic dysregulation, cardiovascular risk, impaired quality of life, and psychological morbidity [,]. The pathophysiology of MOSH is multifactorial and bidirectional. Adipose tissue hypertrophy increases the expression and activity of aromatase (CYP19A1), the enzyme responsible for peripheral conversion of testosterone to oestradiol, thereby creating a negative feedback loop that suppresses gonadotropin-releasing hormone (GnRH) pulsatility and, consequently, luteinising hormone (LH) secretion [,]. Concurrently, obesity-associated hyperinsulinaemia and insulin resistance reduce hepatic synthesis of sex hormone-binding globulin (SHBG), further diminishing bioavailable testosterone fractions []. Systemic low-grade inflammation—characterised by elevated IL-6, TNF-α, and CRP—exerts direct inhibitory effects on Leydig cell steroidogenesis [,]. The ‘Gut Endotoxin Leading to a Decline IN Gonadal function’ (GELDING) theory has been proposed as an additional mechanistic pathway, suggesting that obesity-induced intestinal dysbiosis and lipopolysaccharide (LPS) translocation may compromise testicular function []; however, direct causal evidence in humans remains limited, and this mechanism warrants further prospective investigation before definitive conclusions can be drawn. Given the reversible nature of MOSH—in contrast to organic hypogonadism—lifestyle interventions, particularly dietary modifications, represent the primary therapeutic strategy before considering testosterone replacement therapy (TRT) [,]. Weight loss of 5–10% of body weight has been associated with clinically meaningful testosterone increments, and the magnitude of hormonal recovery appears proportional to the degree of weight reduction [,]. However, the optimal dietary approach to maximise testosterone restoration in obese men remains undefined.