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The corticosteroids are steroid hormones produced by the adrenal cortex. They consist of two major physiologic and pharmacologic groups: (1) glucocorticoids, which have important effects on carbohydrate, fat and protein metabolism, catabolism, immune responses, and inflammation; and (2) mineralocorticoids, which regulate sodium and potassium reabsorption in the collecting tubules of the kidney. This chapter reviews the glucocorticoids, the mineralocorticoids, and the corticosteroid antagonists.



A. Mechanism of Action

Corticosteroids enter the cell and bind to cytosolic receptors that transport the steroid into the nucleus. The steroid-receptor complex alters gene expression by binding to glucocorticoid response elements (GREs) or mineralocorticoid-specific elements (Figure 39–1). Tissue-specific responses to steroids are made possible by the presence in each tissue of different protein regulators that control the interaction between the hormone-receptor complex and particular DNA response elements.


Mechanism of glucocorticoid action. This figure models the interaction of a steroid (S; eg, cortisol), with its receptor (R) and the subsequent events in a target cell. The steroid is present in the blood bound to corticosteroid-binding globulin (CBG) but enters the cell as the free molecule. The intracellular receptor is bound to stabilizing proteins, including heat shock protein 90 (Hsp90) and several others (X). When the complex binds a molecule of steroid, the Hsp90 and associated molecules are released. The steroid-receptor complex enters the nucleus as a dimer, binds to the glucocorticoid response element (GRE) on the gene, and regulates gene transcription. The resulting mRNA is edited and exported to the cytoplasm for the production of protein that brings about the final hormone response. (Reproduced with permission from Katzung BG, Vanderah TW: Basic & Clinical Pharmacology, 15th ed. New York, NY: McGraw Hill; 2021.)

B. Organ and Tissue Effects

1. Metabolic effects

Glucocorticoids stimulate gluconeogenesis. As a result, blood glucose rises, muscle protein is catabolized, and insulin secretion is stimulated. Both lipolysis and lipogenesis are stimulated, with a net increase of fat deposition in certain areas (eg, the face and the shoulders and back).

2. Catabolic effects

Glucocorticoids cause muscle protein catabolism. In addition, lymphoid and connective tissue, fat, and skin undergo wasting under the influence of high concentrations of these steroids. Catabolic effects on bone can lead to osteoporosis. In children, growth is reduced.

3. Immunosuppressive effects

Glucocorticoids inhibit cell-mediated immunologic functions, especially those dependent on lymphocytes. These agents are actively lymphotoxic and, as such, are important in the treatment of hematologic cancers. The drugs do not interfere with the development of normal acquired immunity but delay rejection reactions in patients with organ transplants.

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