PMID- 17950991
OWN - NLM
STAT- MEDLINE
DCOM- 20080208
LR  - 20131121
IS  - 0303-7207 (Print)
IS  - 0303-7207 (Linking)
VI  - 279
IP  - 1-2
DP  - 2007 Dec 15
TI  - Corticosterone has direct inhibitory effect on the expression of peptide hormone 
      receptors, 11 beta-HSD and glucose oxidation in cultured adult rat Leydig cells.
PG  - 52-62
AB  - The present study was designed to investigate the dose-dependent direct effect of 
      corticosterone on the expression of peptide hormone receptors, 11 
      beta-hydroxysteroid dehydrogenase (11 beta-HSD) and glucose oxidation in cultured 
      adult rat Leydig cells. Leydig cells were isolated from the testis of normal 
      adult male albino rats, purified on discontinuous Percoll gradient and plated in 
      culture plates/flasks overnight at 34 degrees C in a CO(2) incubator under 95% 
      air and 5% CO(2) using DME/F12 medium containing 1% fetal bovine serum. After the 
      attachment of cells, serum containing medium was removed and cells were exposed 
      to different doses (0, 50, 100, 200, 400 and 800 nM) of corticosterone using 
      serum-free fresh medium for 24h at 34 degrees C. At the end of exposure period, 
      cells were utilized for the quantification of cell-surface LH, prolactin, insulin 
      receptors and their mRNA expression, the activity and mRNA expression of 11 
      beta-HSD and glucose oxidation. Testosterone production was estimated in cell 
      pellets and in culture media. At all doses employed, corticosterone significantly 
      decreased the production of testosterone by Leydig cells. The concentration of 
      cell-surface LH and prolactin receptors were significantly reduced after 
      corticosterone exposure whereas the concentration of insulin receptor was 
      diminished only at 200-800 nM doses of corticosterone. The levels of LH and 
      prolactin receptor mRNAs were significantly decreased after corticosterone 
      (100-800 nM) exposure whereas the mRNA level of insulin receptor was 
      significantly reduced only at 800 nM dose of corticosterone. 11 beta-HSD mRNA 
      expression as well as the activity was significantly inhibited by corticosterone 
      treatment. Glucose oxidation was markedly inhibited by corticosterone exposure in 
      a dose-dependent manner. It is concluded from this in vitro study that 
      corticosterone induces steroidogenic lesion in testicular Leydig cells by 
      decreasing the number of cell-surface LH, prolactin and insulin receptors, the 
      activity of 11 beta-HSD and their mRNA levels and glucose oxidation.
FAU - Rengarajan, Srinivasan
AU  - Rengarajan S
AD  - Department of Endocrinology, Dr. ALM Post-Graduate Institute of Basic Medical 
      Sciences, University of Madras, Taramani Campus, Chennai 600113, India.
FAU - Balasubramanian, Karundevi
AU  - Balasubramanian K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070906
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (Receptors, Peptide)
RN  - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
RN  - IY9XDZ35W2 (Glucose)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - 11-beta-Hydroxysteroid Dehydrogenases/antagonists & inhibitors/*drug 
      effects/metabolism
MH  - Animals
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Corticosterone/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Glucose/*metabolism
MH  - Leydig Cells/drug effects/*metabolism
MH  - Male
MH  - Molecular Sequence Data
MH  - Oxidation-Reduction
MH  - Rats
MH  - Receptors, Peptide/antagonists & inhibitors/*drug effects/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2007/10/24 09:00
MHDA- 2008/02/09 09:00
CRDT- 2007/10/24 09:00
PHST- 2007/04/24 00:00 [received]
PHST- 2007/07/11 00:00 [revised]
PHST- 2007/09/03 00:00 [accepted]
PHST- 2007/10/24 09:00 [pubmed]
PHST- 2008/02/09 09:00 [medline]
PHST- 2007/10/24 09:00 [entrez]
AID - S0303-7207(07)00338-3 [pii]
AID - 10.1016/j.mce.2007.09.001 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 2007 Dec 15;279(1-2):52-62. doi: 10.1016/j.mce.2007.09.001. 
      Epub 2007 Sep 6.