Adrenal Cortex Secretion and Glucocorticoid Functions

Adrenal Cortex Secretion Control

Control of secretion by the adrenal cortex is regulated by the hypothalamic-pituitary axis. Various other mechanisms also influence the release of adrenal cortical hormones.

Negative Feedback and ACTH Regulation

The regulation of ACTH secretion involves a negative feedback mechanism centered on cortisol and its derivative, cortisone. An increase in cortisol levels inhibits ACTH secretion, while a drop stimulates it. Furthermore, an excess of cortisol leads to a decrease in Corticotropin-Releasing Factor (CRF).

Circadian Rhythm of Cortical Hormones

The levels of adrenal cortical hormones depend on circadian rhythms and can be influenced by certain drugs. Cortisol exhibits a marked circadian rhythm, reaching its highest concentration in the morning and its lowest at night. This rate is independent of the hypothalamic-pituitary feedback shown in the adrenal glands.

Aldosterone Release Mechanisms

The release of aldosterone is controlled by two primary mechanisms, including renal clearances. The hypothalamic-pituitary axis also acts on aldosterone production through the following:

• ACTH: Maintains the growth and synthetic capacity of the zona glomerulosa and increases aldosterone production.
• CRF: Triggers the release of both ACTH and aldosterone.
• Limbic System: Regulates CRF secretion, which subsequently affects aldosterone levels.

Biological Actions of Glucocorticoids

These hormones act on intermediary metabolism across many tissues and organs.

Carbohydrate Metabolism Effects

The effects of cortisol on carbohydrate metabolism result in increased blood glucose levels, acting as a hyperglycemic and anti-insulin hormone. Cortisol achieves this through:

• Activation of key enzymes involved in gluconeogenesis.
• Induction of hepatic synthesis.
• Inhibition of glycolysis by decreasing the activity of key glycolytic enzymes.

Lipid Metabolism and Lipolysis

Glucocorticoids are lipolytic hormones. While cortisol promotes lipolysis, its effects vary by tissue:

• Fatty Acid Mobilization: Glucocorticoids favor the mobilization of fatty acids from adipose tissue.
• Inhibition of Re-esterification: By blocking glucose utilization, they inhibit the re-esterification of fatty acids.
• Hepatic Oxidation: In the liver, glucocorticoids stimulate fatty acid oxidation and favor gluconeogenesis by increasing available substrates and activating gluconeogenic enzymes.

Protein Metabolism and Amino Acid Regulation

Cortisol promotes the degradation of proteins in various tissues, leading to the release of amino acids. This process includes:

• Urea Cycle Acceleration: Increased amino group elimination leads to higher urea production.
• Hepatic Protein Formation: In the liver, cortisol favors the formation of proteins.
• Peripheral Inhibition: In peripheral tissues, it inhibits protein translation and synthesis.