Differential response of Leydig cells in expressing 11β-HSD type I and cytochrome P450 aromatase in male rats subjected to corticosterone deficiency

Chandrakesan Parthasarathy, Yuvaraj Sambandam, Ramachandran Ilangovan, Panneerselvam Janani, Palaniyandi Kanagaraj, Muthusamy Balaganesh, Bhaskaran Natarajan, Sivanandane Sittadjody, Karundevi Balasubramanian*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Emerging evidence suggests that the glucocorticoid and estradiol are important for Leydig cell steroidogenesis and are regulated via aromatase for estradiol production and 11β-HSD for oxidatively inactivating glucocorticoid. Although it is known that corticosterone deficiency impaired Leydig cell steroidogenesis, its effect on the expression of Leydig cell 11β-HSD type I and aromatase are yet to be recognized. Following metyrapone-induced corticosterone deficiency, serum corticosterone and testosterone levels decrease, whereas serum estradiol remains unaltered. 11β-HSD type I mRNA and its activity was decreased by corticosterone deficiency, whereas the activity and mRNA of aromatase remains unaltered. Simultaneous administration of corticosterone prevented its deficiency-induced changes of 11β-HSD type I in Leydig cells. Our results show that metyrapone-induced corticosterone deficiency impairs Leydig cell 11β-HSD enzyme activity and 11β-HSD type I mRNA expression, and the Leydig cells need to maintain their intracellular concentration of corticosterone for a normal function.

Original languageEnglish (US)
Pages (from-to)18-23
Number of pages6
JournalMolecular and Cellular Endocrinology
Issue number1-2
StatePublished - Nov 13 2009


  • 11β-HSD
  • Aromatase
  • Corticosterone deficiency
  • Leydig cell
  • mRNA expression

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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