Adrenal Cortex Hormone Secretion and Regulation

Regulation of Secretion in the Adrenal Cortex

The adrenal cortex is primarily controlled by the hypothalamic-pituitary axis. However, other mechanisms also influence the release of adrenal cortical hormones.

Negative Feedback

The primary feedback mechanism involves the hormone cortisol and its derivative, cortisone. An increase in cortisol levels inhibits Adrenocorticotropic Hormone (ACTH) secretion, while a decrease stimulates it. An excess of cortisol also leads to a decrease in Corticotropin-Releasing Factor (CRF).

Circadian Rhythm

The levels of adrenal cortical hormones are dependent on the circadian rhythm. Cortisol, in particular, exhibits a pronounced circadian rhythm, with the highest levels in the morning and the lowest at night. This rhythm is independent of the hypothalamic-pituitary feedback loop, as demonstrated in adrenal glands.

Aldosterone release is controlled by two primary mechanisms: renal clearance and the hypothalamic-pituitary axis. The hypothalamic-pituitary axis influences aldosterone by sustaining growth and ACTH synthesis capacity in the zona glomerulosa, thereby increasing aldosterone production. CRF triggers the release of both ACTH and aldosterone. CRF secretion, regulated by the limbic system, also affects aldosterone secretion.

Glucocorticoids

Glucocorticoids, such as cortisol, influence intermediary metabolism in various tissues and organs.

Carbohydrate Metabolism

Cortisol's effects on carbohydrates primarily involve increasing blood glucose levels, acting as an anti-hyperglycemic hormone, opposing insulin. Cortisol achieves this by influencing enzymes involved in gluconeogenesis and inhibiting glycolysis:

• Activation of key enzymes in gluconeogenesis through the induction of hepatic synthesis.
• Inhibition of key enzymes in glycolysis.

By increasing gluconeogenesis activity, cortisol promotes glucose release into the blood. This process requires the input of specific substrates to the liver.

Lipid Metabolism

Glucocorticoids are lipolytic hormones. However, cortisol's effect on lipolysis varies depending on the tissue:

• Adipose Tissue: Glucocorticoids promote fatty acid mobilization. However, since they also block glucose utilization, they inhibit the re-esterification of fatty acids.
• Liver: Glucocorticoids stimulate fatty acid release in the liver by inhibiting glycolytic enzymes. They promote the oxidation of fatty acids in the liver. This results in the promotion of gluconeogenesis by providing substrates and activating gluconeogenic enzymes while inhibiting key glycolytic enzymes.

Protein Metabolism

Cortisol promotes protein degradation in tissues, leading to the release of amino acids. The removal of the amino group accelerates the urea cycle and increases urea production. Cortisol has adverse effects on protein synthesis. While it promotes protein formation in the liver, it inhibits protein synthesis in peripheral tissues through translation inhibition. Glucocorticoids also exert various effects on other tissues and organs.