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The ratio between the two activities ranges from all glucocorticoid and almost no mineralocorticoid activity (cortisol) to all mineralocorticoid and almost no glucocorticoid activity (aldosterone). Glucocorticoids stimulate the conversion of protein to carbohydrate through gluconeogenesis and promote the storage of carbohydrate as glycogen. The increase in urinary nitrogen after an increase in glucocorticoids is the result of amino acid mobilization from protein and its subsequent breakdown as a source of carbon during gluconeogenesis. Adrenalectomized animals are able to function normally as long as food (ie, free amino acids) is available. Upon starvation, however, these animals cannot mobilize amino acids from muscle or serum protein, indicating that cortisol plays a role in the mobilization process. Prolonged exposure to glucocorticoids leads to a diabetic-like state due to the increase in plasma glucose, while low glucocorticoid concentrations lead to hypoglycemia, decreased glycogen stores, and hypersensitivity to insulin. Glucocorticoids also decrease facilitated uptake of glucose in peripheral tissues to provide more glucose for glycogen formation in the liver. This effect is particularly prevalent in leukocytes and may be a major contributing factor to the rapid elevation in blood glucose after steroid administration. The complex mechanisms for the peripheral effects of glucocorticoids are still unclear, but chronic administration can result in the atrophy of lymphatic tissue and muscle, osteoporosis, and thinning of the skin. There are two established effects of glucocorticoids on lipid metabolism. One is the redistribution of body fat in hypercorticism; the other is facilitation of effects of lipolytic agents, steroids direct online. Large doses of glucocorticoids lead to redistribution of fat to the upper trunk and face, with a concomitant loss of fat in the extremities. Therefore, glucose and triglyceride accumulation would occur in response to the rise in insulin levels. Fat cells containing higher levels of receptor (perhaps in the periphery) would respond to the high glucocorticoid level by decreasing glucose uptake and would not accumulate triglycerides. Alternatively, cells in the extremities may be less sensitive to insulin. Electrolyte and Water Balance. The major effect of mineralocorticoids is the regulation of electrolyte excretion in the kidney. Similar effects on cation transport in most other tissues account for all the systemic activity of mineralocorticoids. The primary features of mineralocorticoid excess are positive sodium balance, increased extracellular fluid volume, normal or slightly high plasma sodium, hypokalemia, and alkalosis. Hypocorticism results in renal loss of sodium, hyponatremia, hyperkalemia, and a decrease in extracellular fluid volume and cellular hydration. The 1% decrease in sodium reabsorption that occurs in hypocorticism is enough to cause profound cardiovascular changes, resulting in circulatory collapse, renal failure, and, ultimately, death. Aldosterone modulates sodium levels by activating mineralocorticoid receptors in the distal tubules of the kidney, leading to increased permeability of the apical membrane of the cells lining the cortical collecting tube. However, there is also evidence for a rapid (within minutes) upregulation of sodium-hydrogen exchange by aldosterone that is independent of traditional mineralocorticoid receptors. Mineralocorticoids also increase calcium and magnesium excretion, probably due to volume expansion. Prolonged aldosterone treatment results in sodium ‘escaping,’ a cessation of sodium changes, while potassium and hydrogen loss continues to occur.
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