CORTICOSTERONE: FUNCTIONS AND DISEASES - ANATOMY AND PHYSIOLOGY - 2025

The corticosterone is a hormone that belongs to the family of glucocorticoids. It is considered responsible for regulating the metabolism of fats, proteins and carbohydrates. It is also responsible for some immune reactions and responses to stress.

The hormone corticosterone is produced from cholesterol in the zona fascicular of the cortex of the adrenal glands. When synthesized molecularly, its chemical formula is C ₂₁ H ₃₀ O _4. Unlike cortisol, the main glucocorticoid, this hormone acts as a glucocorticoid and also slightly acts as a mineralocorticoid.

Corticosterone is the hormone responsible for responses to stress

Despite being necessary for some metabolic processes, it is considered of modest importance in humans. Corticosterone has a production of only 2 to 5 mg per day with a plasma concentration of 1-2 µg / dL, while the daily production of cortisol is 10 to 20 mg per day with a concentration of 10-20 µg / dL.

That is, corticosterone circulates in the bloodstream at levels 10 to 20 times lower than cortisol. However, a relative postmortem increase has been evidenced in cuts made from brain samples. In some species of animals, such as rodents, corticosterone is the main hormone in metabolism.

Even though cortisol is the predominant glucocorticoid, corticosterone remains an essential intermediate in mineralocorticoid synthesis. The importance of corticosterone in humans lies in the fact that this is the precursor hormone for aldosterone.

Corticosterone is converted to aldosterone by the enzyme aldosterone synthetase. This compound acts in the conservation of sodium, in the secretion of potassium and in the increase of the arterial pressure.

How is corticosterone made?

The hormone is only synthesized and released in stressful situations, being the cause of episodes known as "stress paralysis", such as those presented in stage fright or when a person refers to being blank from fear.

Stress can be caused by a psychological event (fear, worry, anxiety) or it can be physical (hypoglycemia, pain, infections). When present, the pituitary-adrenal axis and the autonomic nervous system are activated.

The hypophysosadrenal axis starts by activating the hypothalamus, which secretes the hormone corticotropin. This hormone acts on the anterior pituitary and causes the secretion of adenocorticotropic hormone.

The adenocorticotropic hormone then stimulates the adrenal glands, where adrenal steroidogenesis occurs. This synthesizes and releases cortisol and corticosterone in the fascicular zone of the adrenal cortex.

Function

Due to its lipid (cholesterol) nature, corticosterone can cross the blood-brain barrier. Some studies carried out show evidence that suggests that corticosterone influences the neurophysiology of limbic cells by modifying synaptic transmission and ion channels.

It plays a minor role relative to cortisol in the regulation of the immune system and in some metabolic functions, such as the processing of fats, proteins and carbohydrates.

It aids in metabolism by converting amino acids into carbohydrates to use as fuel for many bodily functions. Likewise, it works with the liver to produce glycogen, which can be used as an energy source.

It is converted to aldosterone in the mitochondria of the glomerulosa cells in the adrenal cortex. Unlike other steroid hormones, it is not used as an anti-inflammatory.

It has been linked to an inability to process information and access memory in peak stress situations.

Some studies explain this mechanism by blood redistribution and the start of the gluconeogenesis process towards the main muscle groups, which prepare the body for "flight" thanks to the action of cortisol.

Mechanism of action

These steroids operate through mineralocorticoid receptors and glucocorticoid receptors. Corticosterone is bound to plasma proteins and has a half-life of 50 minutes; it can bind to the transporter protein also called transcortin, with 100% affinity, thus displacing cortisol.

In situations of psychological stress, the brain prepares itself to escape and solve the current problem, "forgetting" any previous information considered by it as irrelevant, which produces the phenomenon of paralysis of fear.

Glucocorticoids provide the necessary energy to muscles to effect the stress response. However, thanks to negative feedback, when there is a large amount of corticosterone in the blood, it sends the information to the hypothalamus to stop the release of corticotropin.

When there is chronic stress

If a situation of chronic stress is established, glucocorticoids inhibit protein synthesis and will begin to break down the muscles to provide amino acids, causing muscle loss and weakness.

Likewise, they interfere with gastric prostaglandin synthesis, breaking down the normal protective barrier against gastric acid and pepsin, causing gastritis and ulcers.

By increasing gluconeogenesis, hyperglycemia can occur, which increases insulin and can accentuate the deposit of fat in the abdomen, face and neck. Likewise, it stimulates the appetite, all of which contribute to weight gain.

Corticosterone-related diseases

The excessive secretion of glucocorticoids, due to their role in increasing blood glucose, is related to some types of diabetes.

Continuously elevated levels can impede the action of other steroid hormones and impair fertility. Similarly, studies have shown that neuronal failure in people with diabetes is related to high levels of corticosterone in the body.

References

1. Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th edition, p1437
2. Goldman L; Ausiello D (Editors). Cecil: Treatise on Internal Medicine. Volume II. 23rd ed. Barcelona: Elsevier Saunders; 2009.
3. F. Dallman. Chronic stress-induced effects of corticosterone on the brain: direct and indirect. Annals of the new york academy of sciences. January 16, 2006. Recovered from: onlinelibrary.wiley.com
4. Gary R. Bortolotti. Tracking stress: localization, deposition and stability of corticosterone in feathers. The Journal of Experimental Biology 212, 1477-1482. Published by The Company of Biologists 2009 doi: 10.1242 / jeb.022152 Recovered from: usask.ca
5. Department of Physiological Sciences. Pontifical Javeriana University. Bogota Recovered from: med.javeriana.edu.co