Hydroxysteroid dehydrogenase

About: Hydroxysteroid dehydrogenase is a research topic. Over the lifetime, 1087 publications have been published within this topic receiving 28468 citations. The topic is also known as: hydroxysteroid dehydrogenase.

Strain-specific differences in the regulation of the hepatic cytoplasmic 17β-hydroxysteroid dehydrogenase activity of the rat

Abstract: 1. 1. The effect of prepuberal gonadectomy of Sprague-Dawley/NIH/HAN rats on cytoplasmic 17β-hydroxysteroid dehydrogenase was examined on day 30, 45, 60, 75, 90 and 105 of life. 2. 2. The activity in male rats was not significantly affected by gonadectomy, whereas the activity in females showed an age-dependent oestrogen dependency. 3. 3. This age-dependent oestrogen dependency could also be demonstrated in 5α-dihydrotestosterone treated intact females. 4. 4. Cytoplasmic 17β-hydroxysteroid dehydrogenase activity of female Chbb:THOM rats also showed an age-dependent oestrogen dependency, whereas the enzyme activity of male rats of this strain showed a distinct androgen dependency absent in Sprague-Dawley/NIH/HAN rats. 5. 5. On the basis of previous investigations it is concluded that the androgen dependency of the enzyme activity of male Chbb:THOM rats has been bred into this strain in the period 1974–1977.

Heterocyclic compound having inhibitory activity on 11-?-hydroxysteroid dehydrogenase type i

Abstract: Discloses 11-hydroxy-β- dehydrogenase Claim useful, the following compounds or a pharmaceutically acceptable salt thereof, or the compound or salt of solvate thereof represented by the following formula as inhibitors of type I: (Of, R

A urine concentrating defect in 11β-Hydroxysteroid Dehydrogenase Type 2 knockout mice

Abstract: Evans LC, Livingstone DE, Kenyon CJ, Jansen MA, Dear JW, Mullins JJ, Bailey MA. A urine-concentrating defect in 11 -hydroxysteroid dehydrogenase type 2 null mice. Am J Physiol Renal Physiol 303: F494 –F502, 2012. First published May 23, 2012; doi:10.1152/ajprenal.00165.2012.—In aldosterone target tissues, 11 -hydroxysteroid dehydrogenase type 2 (11 HSD2) is coexpressed with mineralocorticoid receptors (MR) and protects the receptor from activation by glucocorticoids. Null mutations in the encoding gene, HSD11B2, cause apparent mineralocorticoid excess, in which hypertension is thought to reflect volume expansion secondary to sodium retention. Hsd11b2 / mice are indeed hypertensive, but impaired natriuretic capacity is associated with significant volume contraction, suggestive of a urine concentrating defect. Water turnover and the urine concentrating response to a 24-h water deprivation challenge were therefore assessed in Hsd11b2 / mice and controls. Hsd11b2 / mice have a severe and progressive polyuric/polydipsic phenotype. In younger mice ( 2 mo of age), polyuria was associated with decreased abundance of aqp2 and aqp3 mRNA. The expression of other genes involved in water transport (aqp4, slc14a2, and slc12a2) was not changed. The kidney was structurally normal, and the concentrating response to water deprivation was intact. In older Hsd11b2 / mice ( 6 mo), polyuria was associated with a severe atrophy of the renal medulla and downregulation of aqp2, aqp3, aqp4, slc14a2, and slc12a2. The concentrating response to water deprivation was impaired, and the natriuretic effect of the loop diuretic bumetanide was lost. In older Hsd11b2 / mice, the V2 receptor agonist desmopressin did not restore full urine concentrating capacity. We find that Hsd11b2 / mice develop nephrogenic diabetes insipidus. Gross changes to renal structure are observed, but these were probably secondary to sustained polyuria, rather than of developmental origin.