Figure 1.

Endocrinopathies and male reproduction. (A) Neuroendocrine regulation by hypothalamic–pituitary–gonadal (HPG) axis maintains the normal secretion and functions of reproductive hormones. Gonadotropin-releasing hormone (GnRH) is synthesized by the hypothalamus, which stimulates the anterior pituitary to secrete the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Whereas, gonadotropin-inhibitory hormone (GnIH) inhibits the anterior pituitary gonadotropin synthesis and release. In Leydig cells, LH acts to aid steroidogenesis. FSH acts on the Sertoli cells, supporting spermatogenesis. Sertoli cells secrete activin and inhibin among other substances, which mediate positive and negative feedback on the HPG axis, respectively. (B) Hormonal disturbances owing to endocrinopathies can impair hormonal crosstalk, thereby disrupting essential male reproductive functions. Upregulation of aromatase CYP19 (Cytochrome P450 Family 19) gene leads to a higher conversion rate of testosterone to estrogen, inducing estrogen excess, which in turn inhibits the HPG axis. Hyperprolactinemia is characterized by high serum prolactin levels that impede GnRH release from the hypothalamus, reducing gonadotropin secretion and perhaps inhibiting gonadotropin actions on the gonads. Endocrinopathies including obesity, thyroid hormone imbalance, and diabetes mellitus disrupt the intricate metabolic balance, elicit various metabolic hormones and inflammatory mediators, and may induce oxidative stress, all of which adversely affect the normal endocrine crosstalk regulating male reproductive functions.