M04.10.001 Hypothalamic pitutary gonaldal axis in males

Learning Objective

Understand the hormonal regulation of male reproductive function by describing the roles of the hypothalamus, anterior pituitary, and testes, including feedback mechanisms and the molecular basis of glycoprotein hormone specificity.


Overview of the HPG Axis

The hypothalamic–pituitary–gonadal (HPG) axis regulates testosterone production and spermatogenesis in adult males.
It functions through a coordinated endocrine feedback loop involving:

  • Hypothalamus
  • Anterior pituitary gland
  • Testes (Leydig and Sertoli cells)


Hypothalamic Regulation

The hypothalamus secretes Gonadotropin-Releasing Hormone (GnRH) in a pulsatile manner. Pulsatility is essential because
continuous GnRH exposure leads to downregulation of GnRH receptors on pituitary gonadotrophs. GnRH travels via the hypophyseal portal system to stimulate the anterior pituitary.


Pituitary Hormones

In response to GnRH, the anterior pituitary releases:

  • Luteinizing Hormone (LH)
  • Follicle-Stimulating Hormone (FSH)

These are collectively known as gonadotropins.

LH Function

LH acts on Leydig cells in the testes to stimulate
production of testosterone.

FSH Function

FSH acts on Sertoli cells, promoting:

  • Spermatogenesis
  • Production of Androgen-binding protein (ABP)
  • Secretion of Inhibin B

Activity


Testicular Hormones and Feedback

Testosterone

Testosterone exerts:

  • Anabolic effects
  • Development of secondary sexual characteristics
  • Maintenance of libido
  • Support of spermatogenesis

It provides negative feedback to both the hypothalamus (decreasing GnRH) and the anterior pituitary (decreasing LH).

Inhibin B

Produced by Sertoli cells, inhibin B specifically inhibits FSH secretion via negative feedback at the pituitary.

 


Activity


Glycoprotein Hormone Structure 

LH, FSH, TSH, and human chorionic gonadotropin (hCG) are glycoprotein hormones that share:

  • Identical alpha subunits
  • Distinct beta subunits (which confer receptor specificity)

This structural similarity explains why hCG can stimulate LH receptors, as seen in certain tumors and during pregnancy.


Activity


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