PMID- 7964310
OWN - NLM
STAT- MEDLINE
DCOM- 19941227
LR  - 20190709
IS  - 0022-0795 (Print)
IS  - 0022-0795 (Linking)
VI  - 143
IP  - 1
DP  - 1994 Oct
TI  - Opposite effects of glucocorticoid on hepatic 11 beta-hydroxysteroid 
      dehydrogenase mRNA and activity in fetal and adult sheep.
PG  - 121-6
AB  - The level of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) mRNA in the fetal 
      sheep liver increases dramatically between day 130 and term (term = day 145), but 
      the causal factors remain unknown. The present study was designed to determine 
      the effects of exogenous glucocorticoid on the fetal hepatic 11 beta-HSD gene 
      expression. Dexamethasone (dex; 2 micrograms/min over 15 min every 2 h) or saline 
      was infused into chronically-catheterized fetal sheep at day 130 of gestation for 
      4 days. At the end of infusion, the lower right lobe of the liver was collected, 
      total cellular RNA extracted and subjected to Northern blot analysis. It was 
      found that the level of the hepatic 11 beta-HSD mRNA in dex-treated fetuses was 
      about four times higher than that in the saline-treated controls. To examine 
      whether changes occur in the response of hepatic 11 beta-HSD gene expression to 
      glucocorticoids in adulthood, we also treated non-pregnant ewes with dex (10 
      mg/day) for 4 days. By contrast, this treatment regime in adult sheep produced a 
      small but significant decrease in hepatic 11 beta-HSD mRNA levels. We also 
      determined whether age-specific changes in the hepatic level of 11 beta-HSD mRNA 
      following dex treatment were reflected in the level of 11 beta-HSD enzyme 
      activity. Hepatic 11 beta-HSD activity was determined by a standard in vitro 
      conversion assay using cortisol and cortisone as physiological substrates. In 
      both fetal and adult livers, 11-oxoreductase activity (cortisone-->cortisol) was 
      predominant.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Yang, K
AU  - Yang K
AD  - Department of Obstetrics and Gynecology, Lawson Research Institute, University of 
      Western Ontario, St Joseph's Health Centre, London, Canada.
FAU - Berdusco, E T
AU  - Berdusco ET
FAU - Challis, J R
AU  - Challis JR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 0 (RNA, Messenger)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - EC 1.1.- (Hydroxysteroid Dehydrogenases)
RN  - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
RN  - V27W9254FZ (Cortisone)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - 11-beta-Hydroxysteroid Dehydrogenases
MH  - Animals
MH  - Blotting, Northern
MH  - Cortisone/metabolism
MH  - Dexamethasone/*pharmacology
MH  - Enzyme Activation/drug effects
MH  - Female
MH  - Gene Expression
MH  - Hydrocortisone/metabolism
MH  - Hydroxysteroid Dehydrogenases/*genetics/metabolism
MH  - Liver/drug effects/embryology/*enzymology
MH  - RNA, Messenger/*analysis
MH  - Sheep/*embryology
EDAT- 1994/10/01 00:00
MHDA- 1994/10/01 00:01
CRDT- 1994/10/01 00:00
PHST- 1994/10/01 00:00 [pubmed]
PHST- 1994/10/01 00:01 [medline]
PHST- 1994/10/01 00:00 [entrez]
AID - 10.1677/joe.0.1430121 [doi]
PST - ppublish
SO  - J Endocrinol. 1994 Oct;143(1):121-6. doi: 10.1677/joe.0.1430121.