The glucocorticoids increase blood glucose and liver glycogen levels by stimulating gluconeogenesis. The source of this augmented carbohydrate production is protein, and the protein catabolic actions of the gluco-corticoids result in a negative nitrogen balance. The inhibition of protein synthesis by glucocorticoids brings about a transfer of amino acids from muscle and bone to liver, where amino acids are converted to glucose.
Supraphysiological concentrations of glucocorticoids will induce the synthesis of specific proteins in various tissues. For instance, glucocorticoids stimulate the synthesis of enzymes involved in glucose and amino acid metabolism, including glucose 6-phosphatase and tyrosine transaminase. The relation of this action of glu-cocorticoids to their overall effects on general metabolic processes remains obscure, although the latency of their therapeutic actions (several hours) is consistent with the fact that steroids regulate RNA and protein synthesis.
Glucocorticoids not only break down protein but also stimulate the catabolism of lipids in adipose tissue and enhance the actions of other lipolytic agents. This occurrence results in an increase in plasma free fatty acids and an enhanced tendency to ketosis. The mechanism of this lipolytic action is unknown. The net effect of the biochemical changes induced by the glucocorti-coids is antagonism of the actions of insulin. These biochemical events promote hyperglycemia and glycosuria, which are similar to the diabetic state.
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