When cortisol is produced in response to ACTH, it has negative feedback effects on various elements of the hormonal cascade system that starts in the brain’s cortex; see Figure 1. There is a long feedback loop of cortisol (GC) that is initiated by cortisol release from the adrenal’s zona fasciculata which then travels through the entire circulatory system to partner with the glucocorticoid receptor in target cells. Some cortisol will cross the blood-brain barrier and send a (−) signal to both the brain cortex and the hippocampus, so that the hypothalamus diminishes the CRH signal sent from the hypothalamus to the pituitary. This then lowers the rate of secretion of ACTH by the pituitary. The overall feedback inhibition of ACTH is implemented very rapidly. The feedback on the hippocampus may shut off further electrical activity responsible for the release of CRH and the subsequent release of ACTH. These actions are mediated by glucocorticoid nuclear receptors located in these cells that operate transcriptionally.

Fig1. Communication of the brain cortex, via the hippocampus, hypothalamus, and the pituitary, with the zona fasciculata of the adrenal glands to produce ACTH, which in turn stimulates the production of glucocorticoids. The glucocorticoids (cortisol and corticosterone) which move through the circulatory system of the body bind to their nuclear receptor protein in target cells, which produces a wide variety of biological responses. One example is in the muscle and fat cells. See Figure 2 where cortisol binds to its nuclear receptor and exports glucose to the liver cell and maximizes glycogen storage there. Here GC (glucocorticoids) generate a collective negative feedback in the brain’s cortex, hippocampus, hypothalamus, and pituitary. Also the consequences of an individual’s exposure to stress (hemorrhage, pain, infections, emotions, or cold, etc.) stimulate the production of ACTH. Adrenocorticotropic hormone (ACTH), also known as corticotropin (CRH), is a polypeptide tropic hormone that is secreted by the anterior pituitary gland, which travels through the circulatory system to the adrenal gland’s cortex zona fasciculata region.

Fig2. Cell-specific actions of cortisol on muscle, liver, and fat cells. Cortisol in muscle cells inhibits protein synthesis and in fat cells inhibits lipogenesis. Cortisol, acting through its nuclear receptor in muscle cells, inhibits protein synthesis and stimulates proteolysis which produces free amino acids that will be transmitted via the circulatory system to liver cells and converted to glycogen. Similarly, cortisol and its receptor in fat cells inhibits lipogenesis which is the process of acquiring blood glucose and storing it as fat. Cortisol also stimulates lipolysis, the breakdown of the triglycerides to free fatty acids and glycerol. The fatty acids will subsequently be transferred through the circulatory system to liver cells and stored as glycogen. Both the fatty acids and the amino acids will subsequently be transferred through the circulatory system to liver cells and stored as glycogen.

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مواضيع ذات صلة

Glucocorticoids and Stress

Transport of Glucocorticoids in the Blood (CBG)

Integrated Actions of 1α,25(OH)2D3, PTH, Calcitonin, and FGF23 on Bone Remodeling and Calcium Homeostasis

Calcitonin Receptor and Biological Actions

Parathyroid Hormone-Related Protein Receptor and Biological Actions

Parathyroid Hormone Receptor and Biological Actions

T3 Inhibition of TSH and TRH Gene Expression

Mechanism of T3 Action

Role of Thyroid Hormone in Thermogenesis

Metabolism of Thyroid Hormone :Deiodination

Thyroid Hormone Transporters

Ghrelin, Leptin, and Energy Use