Introduction

The primary regulator of testicular function is gonadotropin-releasing hormone (GnRH) that is secreted episodically by hypothalamic neurons into the portal vascular system. GnRH stimulates the synthesis and secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which are produced by gonadotrophs of the anterior pituitary. LH stimulates testosterone synthesis after binding to specific receptors on Leydig cells, whereas Sertoli cells in the seminiferous tubules are the primary target of FSH (1,2). Accordingly, mass lesions and other disorders of the suprasellar region or pituitary that disrupt GnRH or LH/FSH production result in impaired testicular function that is designated hypogonadotropic hypogo-nadism because of the deficiency of LH and FSH. These disorders are the subject of this chapter.

From: Male Hypogonadism: Basic, Clinical, and Therapeutic Principles Edited by: S. J. Winters © Humana Press Inc., Totowa, NJ

Pituitary Fsh Axis

Fig. 1. Effects of hyperprolactinemia on hypothalamic-pituitary-testicular axis. ABP, androgen-binding globulin; AEC, aromatase enzyme complex; T, testosterone; DHT: dihydrotestosterone; E, estradiol; 5aR, 5a-reductase.

Fig. 1. Effects of hyperprolactinemia on hypothalamic-pituitary-testicular axis. ABP, androgen-binding globulin; AEC, aromatase enzyme complex; T, testosterone; DHT: dihydrotestosterone; E, estradiol; 5aR, 5a-reductase.

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