Secondary male hypogonadism: A prevalent but overlooked comorbidity of obesity

Abstract

Male hypogonadism associated with obesity is a very prevalent condition and is increasing in parallel with the epidemic prevalence of obesity. Low testosterone levels promote higher fat mass with reduced lean mass. Male hypogonadism is related to an increase in associated cardiometabolic complications, such as hypertension, type 2 diabetes mellitus, the metabolic syndrome, and cardiovascular disease. Its influence as a comorbidity of obesity is becoming more evident and should be evaluated and treated in at-risk patients. Mechanisms involved in this relationship include body composition changes, the presence of adipokines, insulin resistance, and other factors, some of which are still unknown. Weight loss and treatment to replace testosterone levels improve the metabolic profile and quality of life in patients with obesity and hypogonadism; these beneficial effects depend on treatment modality and duration of therapy. The use of testosterone replacement therapy may be indicated, as it has not been shown to increase cardiovascular risk, and retrospective studies suggest a reduction in events in men with metabolic syndrome and type 2 diabetes.

Obesity and Hypogonadism—A Narrative Review Highlighting the Need for High-Quality Data in Adolescents

“…FSH and LH are hormones that regulate sexual development in both males and females. In males, FSH stimulates Sertoli cells to support sperm production and produce androgen-binding protein, which binds testosterone and increases its levels in the seminiferous tubule, which further promotes sperm production [20]. LH is necessary for the production of testosterone by Leydig cells [20].…”

“…In males, FSH stimulates Sertoli cells to support sperm production and produce androgen-binding protein, which binds testosterone and increases its levels in the seminiferous tubule, which further promotes sperm production [20]. LH is necessary for the production of testosterone by Leydig cells [20]. Thus, decreased FSH and LH result in decreased stimulation of Sertoli and Leydig cells, resulting in inadequate support and nourishment to developing spermatozoa and decreased testosterone production, respectively [20].…”

“…LH is necessary for the production of testosterone by Leydig cells [20]. Thus, decreased FSH and LH result in decreased stimulation of Sertoli and Leydig cells, resulting in inadequate support and nourishment to developing spermatozoa and decreased testosterone production, respectively [20]. This effect is seen in males with obesity due to the suppression of the HPG axis seen in obesity.…”

“…The genetic predisposition to having elevated BMI resulted in lower testosterone level, suggesting a causal relationship of obesity in hypogonadism. Reductions in testosterone that result from obesity-related hypogonadism contribute to poor spermatogenesis and impaired development and progression of sexual characteristics [20].…”

“…Male obesity-associated secondary hypogonadism (MOSH) is a diagnosis of exclusion, which is made after the primary causes of hypogonadism have been ruled out. It is defined as a syndrome of the inability to produce adequate amounts of testosterone and/or sperm in males with obesity [20,56]. Table 1 details other syndromes associated with hypogonadism.…”