Hormonal regulation of intestinal 11beta-hydroxysteroid dehydrogenase
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
9399631
DOI
10.1016/s0024-3205(97)00956-9
PII: S0024320597009569
Knihovny.cz E-zdroje
- MeSH
- 11-beta-hydroxysteroiddehydrogenasy MeSH
- hormony kůry nadledvin farmakologie MeSH
- hormony farmakologie MeSH
- hydroxysteroiddehydrogenasy metabolismus MeSH
- inzulin farmakologie MeSH
- krysa rodu Rattus MeSH
- orgánové kultury - kultivační techniky MeSH
- střeva enzymologie MeSH
- trijodthyronin farmakologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 11-beta-hydroxysteroiddehydrogenasy MeSH
- hormony kůry nadledvin MeSH
- hormony MeSH
- hydroxysteroiddehydrogenasy MeSH
- inzulin MeSH
- trijodthyronin MeSH
We have previously demonstrated the developmental increase of the activity of 11beta-hydroxysteroid dehydrogenase (11betaHSD) in the rat ileum which correlated with the developmental surge of plasma concentrations of corticosteroids, thyroid hormones and insulin. To ascertain whether these hormones directly stimulate 11betaHSD activity we used explant cultures of ileum and distal colon. The intestinal segments of young, 7-day-old rats, were cultured 48 hours in the presence of aldosterone (10[-7] M), dexamethasone (10[-7] M), triiodothyronine (10[-7] M) or insulin (10[-7] M) and 11betaHSD activity was evaluated by measuring the conversion of [3H]corticosterone to [3H]11-dehydrocorticosterone. The activity of 11betaHSD was significantly increased following 48 h treatment with dexamethasone and aldosterone, whereas insulin and triiodothyronine were without any effect. Corticosterone oxidation was inhibited by carbenoxolone and progesterone. It is being concluded, that both glucocorticoids and mineralocorticoids but not insulin or triiodothyronine induce intestinal 11betaHSD activity.
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