Linked Life Data

16634330

Source:http://linkedlifedata.com/resource/pubmed/id/16634330

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-4-25
pubmed:abstractText
Clinical and experimental studies have shown the adverse effects of excess glucocorticoid on testicular testosterone production. The NADPH co-enzyme has been recognized as an important factor that regulates several steps in steroidogenesis, while glucose oxidation acts as a limiting factor on testicular testosterone production. Nevertheless, the impact of excess corticosterone, the stress hormone on testicular NADPH availability and glucose oxidation is unknown. Therefore, the present study was designed to assess the specific effects of excess corticosterone on Leydig cell NADPH generating enzymes and glucose oxidation. Adult Wistar rats (200-250 g, b.w.) were treated with corticosterone-21-acetate (2 mg/ 100 g, b.w., i.m., twice daily) for 10 days and corticosterone-21-acetate plus luteinizing hormone (LH) (100 microg/kg b.w., i.m., daily) for 10 days. After the treatment period, experimental animals and controls were killed, blood was collected and the sera separated for testosterone assay. Testes were removed and Leydig cells were isolated, purified and used for estimating the specific activity of NADPH generating enzymes and 14C-glucose oxidation. Serum testosterone, Leydig cellular 14C-glucose oxidation and the specific activities of 6-phosphogluconate dehydrogenase (6-PGDH), NADP-isocitrate dehydrogenase (ICDH) and malic enzyme were significantly decreased in corticosterone-treated rats. Co-administration of LH with corticosterone maintained the specific activities of 6-PGDH and ICDH and 14C-glucose oxidation at control level. Nevertheless, serum testosterone and Leydig cellular malic enzyme activity showed a significant decrease in these rats. In conclusion, the inhibitory effects of excess corticosterone on Leydig cell steroidogenesis are mediated through impaired glucose oxidation and defective NADPH generation. Co-administration of LH with corticosterone failed to prevent the decrease in serum testosterone and Leydig cell malic enzyme activity, suggesting the dominant inhibitory effects of excess corticosterone.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0960-3271
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
119-25
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Effects of excess corticosterone on NADPH generating enzymes and glucose oxidation in Leydig cells of adult rats.
pubmed:affiliation
Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai-600 113, Tamil Nadu, India.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't