Glucocorticoid metabolism and Na+ transport in chicken intestine.

Content Provider	Semantic Scholar
Author	Mazancov́a, Karla Kucka, Marek Pácha, Jiří
Copyright Year	2005
Abstract	The role of aldosterone in regulation of electrogenic Na+ transport is well established, though mineralocorticoid receptors bind glucocorticoids with similar binding affinity as aldosterone and plasma concentration of aldosterone is much lower than glucocorticoids. In mammals, the aldosterone specificity is conferred on the low-selective mineralocorticoid receptors by glucocorticoid inactivating enzyme 11beta-hydroxysteroid dehydrogenase (11HSD) that converts cortisol or corticosterone into metabolites (cortisone, 11-dehydrocorticosterone) with lower affinity for these receptors. The present study examined the chicken intestine, whether changes in 11HSD activity are able to modulate the effect of corticosterone on Na+ transport, and how the metabolism of this hormone is distributed within the intestinal wall. This study shows that not only aldosterone, but also corticosterone (B), was able to increase the electrogenic Na+ transport in chicken caecum in vitro. The effect of corticosterone was higher in the presence of carbenoxolone, an inhibitor of steroid dehydrogenases, and was comparable to the effect of aldosterone. The metabolism of B in the intestine was studied; results showed oxidation of this steroid to 11-dehydrocorticosterone (A) and reduction to 11-dehydro-20beta-dihydrocorticosterone (20diA) as the main metabolic products at low nanomolar concentration of the substrate. In contrast, 20beta-dihydrocorticosterone and 20diA were the major products at micromolar concentration of B. Progesterone was converted to 20beta-dihydroprogesterone. The metabolism of corticosterone was localized predominantly in the intestinal mucosa (enterocytes). In conclusion, the oxidation at position C11 and reduction at position C20 suggest that both 11HSD and 20beta-hydroxysteroid dehydrogenase (20HSD) operate in the chicken intestine and that the mucosa of avian intestine possesses a partly different system of modulation of corticosteroid signals than mammals. This system seems to protect the aldosterone target tissue against excessive concentration of corticosterone and progesterone.
Starting Page	68
Ending Page	72
Page Count	5
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.natureblink.com/publikace/JEZ303.pdf
PubMed reference number	15662663v1
Volume Number	303
Issue Number	2
Journal	Journal of experimental zoology. Part A, Comparative experimental biology
Language	English
Access Restriction	Open
Subject Keyword	11-beta-hydroxysteroid dehydrogenase activity 11-dehydrocorticosterone 20-alpha-Dihydroprogesterone Adrenal Cortex Hormones Affinity Aldosterone Aves Carbenoxolone Corticosterone Cortisone Enterocytes Hydrocortisone Hydroxysteroid Dehydrogenases Hydroxysteroids Intestinal Mucosa Intestinal Wall Tissue Mammals Metabolic Process, Cellular Mineralocorticoid Receptor Mineralocorticoids Mucous Membrane Oxidoreductase Receptors, Progesterone Sodium Steroids oxidation
Content Type	Text
Resource Type	Article