Hydroxysteroid dehydrogenase-like protein 2

When tested in vitro , 7-keto appears to activate the beta subset of the estrogen receptor (ERβ) with an EC 50 around 500μM which is partially blocked by exemestane (aromatase inhibitor or AI); there was no apparent activity on the classical subset (ERα) and parent DHEA and DHEAS were eqipotent. [45] As activity was hindered with an AI and there was efficacy in HepG2 cells but not Hep293 (expressing [46] and not expressing [47] aromatase, respectively) it is though that 7-oxo can be metabolized into an estrogen. [45]

The fetal adrenal cortex lacks expression of the enzyme early on, thus mineralocorticoids (. aldosterone ) and glucocorticoids (. cortisol ) cannot be synthesized. This is significant because cortisol induces type II pneumocytes of the lungs to synthesize and secrete pulmonary surfactant ; without pulmonary surfactant to reduce the alveolar surface tension , premature neonates may die of neonatal respiratory distress syndrome . If delivery is unavoidable (. because of placental abruption , or pre-eclampsia / HELLP syndrome ), then glucocorticoids (. cortisol) can be administered.

"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 an infant with a D-bifunctional protein deficiency ( 261515 ), van Grunsven et al. (1998) identified a 46G-A transition in the HSD17B4 gene, resulting in a gly16-to-ser (G16S) substitution within an important loop of the Rossman fold forming the NAD(+)-binding site. Biochemical analysis showed that the 3-hydroxyacyl-CoA dehydrogenase activity of the D-bifunctional protein was completely inactive, whereas the enoyl-CoA hydratase component was active. Their findings showed that the D-bifunctional protein plays an essential role in the peroxisomal beta-oxidation pathway that cannot be compensated for by the L-specific bifunctional protein. Both parents were heterozygous for the mutation.

Hydroxysteroid dehydrogenase-like protein 2

hydroxysteroid dehydrogenase-like protein 2

In an infant with a D-bifunctional protein deficiency ( 261515 ), van Grunsven et al. (1998) identified a 46G-A transition in the HSD17B4 gene, resulting in a gly16-to-ser (G16S) substitution within an important loop of the Rossman fold forming the NAD(+)-binding site. Biochemical analysis showed that the 3-hydroxyacyl-CoA dehydrogenase activity of the D-bifunctional protein was completely inactive, whereas the enoyl-CoA hydratase component was active. Their findings showed that the D-bifunctional protein plays an essential role in the peroxisomal beta-oxidation pathway that cannot be compensated for by the L-specific bifunctional protein. Both parents were heterozygous for the mutation.

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