Male Reproductive System Overview

Male Reproductive System Overview

• Key Differences: Male and female reproductive systems differ significantly due to steroid hormone levels.
• Male Steroids: Testosterone is the primary androgen; it can be converted to dihydrotestosterone (DHT) or estrogen in certain tissues.
• Female Steroids: Estrogens (multiple types) and progestins are the primary hormones.
• Hormone Ratios: Male systems have a higher androgen-to-estrogen ratio; females have a higher estrogen-to-androgen ratio.
• Secretion Patterns: Female hormone secretion is cyclical (approximately 20-30 days), whereas male testosterone secretion is relatively constant. Both sexes have versatile pituitary and hypothalamic hormone secretion.
• Reproductive Decline: Female reproduction declines dramatically at menopause; male hormone levels and semen production decline less dramatically but still decrease with age.

Hormonal Control of Reproduction

• GnRH (Gonadotropin-Releasing Hormone): Released by hypothalamus; controls LH and FSH release from the pituitary gland.
• LH (Luteinizing Hormone): Acts on Leydig cells (and Thecal Cells) to stimulate steroid hormone production.
• FSH (Follicle-Stimulating Hormone): Acts on Sertoli cells (and Granulosa cells) in the gonads.
• Gonadal Steroid Production: Testosterone is produced in the testes (males); estradiol and progesterone are primary steroids produced in the ovaries (females).
• Feedback Mechanisms: Testosterone in males provides negative feedback to the pituitary and hypothalamus, maintaining relatively constant levels. Estradiol in females causes both negative and positive feedback, resulting in cyclical patterns.

Testicular Structure and Function

• Seminiferous Tubules: Contain Sertoli cells and developing sperm cells; make up most of the testes. Leydig cells are surrounding the Tubules
• Hormonal Actions: LH stimulates testosterone production in Leydig cells; testosterone acts on Sertoli cells and directly on sperm; FSH acts on Sertoli cells.
• Sertoli Cell Functions: Produce nutrients for developing sperm ("nurse cells"); and secrete ABP (Androgen-Binding Protein) which binds and concentrates testosterone in the seminiferous tubule fluid, crucial for sperm maturation. FSH stimulates the production of ABP. Also secretes Inhibin which regulates FSH & LH.
• Spermatogenesis: Sperm maturation occurs as cells move through seminiferous tubules, requiring testosterone.

Mechanisms of Steroid Hormone Action

• General Mechanism: Steroid hormones generally affect gene expression.
• Testosterone Mechanism: Testosterone enters cells, binds to receptors, which dimerize, releasing chaperonin proteins, entering the nucleus, and activating gene transcription.
• DHT (Dihydrotestosterone): Converted from testosterone; binds to androgen receptors even better than testosterone in some tissues.
• Estrogen Formation: Aromatase converts testosterone to estrogen, which binds to estrogen receptors.

Roles of Testosterone and DHT

• Fetus: Fundamental for development of internal (testosterone) and external genitalia (DHT).
• Puberty: Crucial for development of secondary sexual characteristics, body composition, and bone growth.
• Adult Males: Supports spermatogenesis, maintaining bone density, and affecting metabolism. Maintenance of external genitalia and accessory sex organs is dependent on both.
• Five Alpha Reductase Deficiency - Underdevelopment of external genitalia requiring high testosterone levels for puberty.

Ovary Cell Types and Steroid Production

• Thecal Cells: Produce androgens, stimulated by LH.
• Granulosa Cells: Convert androgens to estrogens, stimulated by FSH.
• Key Enzyme: P450 aromatase is crucial for conversion of androgens to estrogens in granulosa cells.

Pathophysiology of Male Sexual Function

• Normal function: Relies on normal hormones, enzyme and receptor expression, adequate blood flow (vasodilation).
• Factors Affecting Function: Hypogonadism (low testosterone/LH/GnRH), low growth hormone, poor perfusion, neuropathies, cirrhosis, exogenous steroid use all can have negative effects
• Effects of Low Testosterone: Loss of muscle mass, increased risk of anemia and osteoporosis, mood changes, and insulin resistance.
• Adverse Effects of Androgen Excess: Increased muscle mass, infertility, adverse lipid profile, increased cardiovascular disease risk, and potential for androgen-dependent cancers (e.g., prostate cancer).