11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action

Other symptoms reported by sufferers include but are not limited to: nausea, vomiting, fatigue, photophobia (dislike of and pain caused by bright light), problems with balance and spatial awareness, aphasia (difficulty using or understanding words), disorientation, loss of short-term memory (sometimes also long-term memory loss), confusion, feeling 'spaced out', decreased depth perception and peripheral vision. Some children are often too young to report their symptoms adequately and can present with many nonspecific symptoms such as mood swings and more. Although many sufferers have symptoms in common, each sufferer is an individual and should be treated accordingly.

"The whole body 11bHSD1 activity reflects mainly hepatic expression. Initial studies that relied on measurements of cortisol-to-cortisone metabolites in urine (23,36) should be taken with caution as indicative of 11bHSD1 activity, because several other cortisol and cortisone metabolizing enzymes are deregulated in obesity (36). Of greater importance is the finding of reduced hepatic 11bHSD1 activity measured by the conversion of orally administered cortisone to cortisol (23,37). Thus, 11bHSD1 upregulation in obesity seems not to be a generalized process. In both the whole body and the splanchnic circulation there are no differences between obese and lean subjects regarding cortisol regeneration rates (as measured by [2H4]-cortisol tracer), presumably because an upregulation in adipose tissue is counterbalanced by a downregulation in the liver (15).

In 2 unrelated patients, Ulick et al. (1979) described a disorder in the peripheral metabolism of cortisol, manifested by hypertension, hypokalemia, low plasma renin activity, and responsiveness to spironolactone. Aldosterone levels were subnormal. Although the features suggested primary mineralocorticoid excess, no overproduction of mineralocorticoid could be demonstrated. One of the patients, who had been reported by New et al. (1977), was a 3-year-old Zuni Indian girl with hypertension, hypokalemia, and decreased secretion of all known sodium-retaining corticosteroids. The second patient was a boy of Middle Eastern parentage who had a stroke with residual left hemiparesis at age 7, and was first found to be hypertensive at age 9 (blood pressure as high as 250/180 mm Hg). Other findings included growth retardation, grade III retinopathy, hypokalemia, and hyposthenuria. Biochemical studies indicated a decreased rate of conversion of active cortisol to cortisone, and the authors postulated a defect in 11-beta-hydroxy oxidation of cortisol. Ulick et al. (1979) suggested the term 'apparent mineralocorticoid excess.'

11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action

11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action

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11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action