Acth steroid synthesis

Because steroids are lipophilic, they diffuse easily through the cell membranes, and therefore have a very large distribution volume. In their target tissues, steroids are concentrated by an uptake mechanism which relies on their binding to intracellular proteins (or " receptors ", see below). High concentration of steroids are also found in adipose tissue, although this is not a target for hormone action. In the human male, adipose tissue contains aromatase activity, and seems to be the main source of androgen-derived estrogens found in the circulation. But most of the peripheral metabolism occurs in the liver and to some extent in the kidneys, which are the major sites of hormone inactivation and elimination, or catabolism (see below).

Caution must be exercised in interpreting test findings. In patients with Cushing's disease, endogenous ACTH and cortisol production should be suppressed with high-dose (8-mg) dexamethasone, but the test lacks specificity, a clear cutoff value and diagnostic accuracy. 3 , 6 , 19 , 24 , 25 In fact, the pretest probability of finding a pituitary cause for ACTH-dependent Cushing's syndrome (85 to 90 percent) may exceed the diagnostic accuracy of the test. 4 , 25 Microadenomas are more likely to demonstrate high-dose dexamethasone suppression than macroadenomas (92 versus 56 percent in one study). 26

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

The uptake, by skeletal muscle, accounts for >70% of the glucose removal from the serum in humans. Therefore, it should be obvious that this event is extremely important for overall glucose homeostasis, keeping in mind, of course, that glucose uptake by cardiac muscle and adipocytes cannot be excluded from consideration. An important fact related to skeletal muscle glucose uptake is that this process is markedly impaired in individuals with type 2 diabetes. The uptake of glucose increases dramatically in response to stress (such as ischemia) and exercise and is stimulated by insulin-induced recruitment of glucose transporters to the plasma membrane, primarily GLUT4. Insulin-independent recruitment of glucose transporters also occurs in skeletal muscle in response to contraction (exercise). The activation of AMPK plays an important, albeit not an exclusive, role in the induction of GLUT4 recruitment to the plasma membrane. In fact, the ability of AMPK to stimulate GLUT4 translocation to the plasma membrane in skeletal muscle occurs via a mechanism distinct from that stimulated by insulin since together insulin and AMPK effects are additive. AMPK activation also results in increased expression of the GLUT4 gene through enhanced binding of the transcription factor MEF-2 (myocyte enhancer factor-2) to promoters in the GLUT4 gene. In addition, there is some demonstration that AMPK may regulate glucose transport through GLUT1. Increased glucose uptake will result in an increase in glycolysis and ATP production.

Acth steroid synthesis

acth steroid synthesis

The uptake, by skeletal muscle, accounts for >70% of the glucose removal from the serum in humans. Therefore, it should be obvious that this event is extremely important for overall glucose homeostasis, keeping in mind, of course, that glucose uptake by cardiac muscle and adipocytes cannot be excluded from consideration. An important fact related to skeletal muscle glucose uptake is that this process is markedly impaired in individuals with type 2 diabetes. The uptake of glucose increases dramatically in response to stress (such as ischemia) and exercise and is stimulated by insulin-induced recruitment of glucose transporters to the plasma membrane, primarily GLUT4. Insulin-independent recruitment of glucose transporters also occurs in skeletal muscle in response to contraction (exercise). The activation of AMPK plays an important, albeit not an exclusive, role in the induction of GLUT4 recruitment to the plasma membrane. In fact, the ability of AMPK to stimulate GLUT4 translocation to the plasma membrane in skeletal muscle occurs via a mechanism distinct from that stimulated by insulin since together insulin and AMPK effects are additive. AMPK activation also results in increased expression of the GLUT4 gene through enhanced binding of the transcription factor MEF-2 (myocyte enhancer factor-2) to promoters in the GLUT4 gene. In addition, there is some demonstration that AMPK may regulate glucose transport through GLUT1. Increased glucose uptake will result in an increase in glycolysis and ATP production.

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