One of the Most Important Functions of Glucocorticoids Is Control of Metabolism, in Particular the Stimulation of Hepatic Gluconeogenesis
The mechanism of action of adrenal hormones is similar to that of other lipophilic hormones: they are able to penetrate the cell membrane and interact in the cytoplasm with specific cytosolic receptors.
This complex is transferred to the nucleus, resulting in transcription of certain genes and the synthesis of specific proteins that affect the biological action of the adrenal hormones.As emphasized previously, adrenocortical hormones are classified as either glucocorticoid or mineralocorticoid in their activity. Before the biological actions of each class are discussed, it is important to realize that there is overlap of activity (Table 34-2). For example, whereas cortisol is the dominant glucocorticoid hormone, it also has mineralocorticoid effects, although at a reduced potency.
The glucocorticoid hormones are important mediators of intermediary metabolism. One of the important specific effects of glucocorticoids is the stimulation of hepatic gluconeogenesis, which involves the conversion of amino acids to carbohydrates. The net result is an increase in hepatic glycogen and a tendency to increase blood glucose levels. These effects on glycogen metabolism are observed mainly in animals that have excessive glucocorticoid secretion (hyperadrenocorticism) or an insulin deficiency. The effect of glucocorticoids on
Table 34-2
Relative Glucocorticoid and Mineralocorticoid Potencies OfVarious Steroids
| Steroid | Glucocorticoid potency (relative to cortisol) | Mineralocorticoid potency | |||||||||||||||||||||
| Cortisol | 1 | 1 | |||||||||||||||||||||
| Aldosterone | 0.1 | 400 | |||||||||||||||||||||
| Corticosterone | 0.2 | 2 | |||||||||||||||||||||
| Il-Deoxycorticosterone | has been termed the anti-insulin effect. The chronic administration of glucocorticoids can lead to the development of a syndrome called steroid diabetes because of the hyperglycemic effect produced at the level of the liver; use of glucose decreases in the peripheral tissues because of insulin antagonism. Whereas the actions of glucocorticoids on fat metabolism tend to be complex, the direct effect on adipose tissue is to increase the rate of lipolysis and to redistribute fat into the liver and abdomen. This fat redistribution leads to the classic “potbelly” appearance of animals and humans with hyper- adrenocorticism. Protein synthesis is inhibited by glucocorticoids; in fact, protein catabolism is enhanced, with an accompanying release of amino acids. This process supports hepatic gluconeogenesis. Two tissues, cardiac and brain, are spared from the effect of glucocorticoids on protein catabolism. Chronic administration of glucocorticoids results in muscle wasting and the weakening of bone. The mobilization and incorporation of amino acids into glycogen result in an increase in urinary excretion of nitrogen and a negative nitrogen balance. Glucocorticoids play a role in water diuresis (i.e., the enhancement of water excretion). Whereas glucocorticoids inhibit vasopressin activity in the distal tubule, the most important effect is to increase the GFR. Table 34-3 summarizes the effects of glucocorticoids. Table 34-3 Glucocorticoid Effects and Target Tissues
From Hedge GA, Colby HD, Goodman RL: Clinical endocrine physiology, Philadelphia, 1987, Saunders.
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