# REGULATION OF ANDROGEN SECRETION IN MAMMALIAN TESTES

> **NIH NIH R01** · JOHNS HOPKINS UNIVERSITY · 1994 · $250,691

## Abstract

The Leydig cell produces testosterone in mammals.  Testosterone is required
for the development of the male reproductive tract, for embryonic and
neonatal "imprinting" of testosterone responsive structures such as the
hypothalamus, prostate and liver, for potency and libido in the adult make,
and for testicular, epididymal and accessory sex organ function in the
adult.  Yet, little is known regarding the factors regulating development
of and sustaining steroidogenic function in Leydig cells.  Therefore, we
propose studies in the neonatal rat designed to:  first, identify
transitional cells intermediate between primitive mesenchymal precursor
cells and the adult Leydig cell; second, describe unequivocal morphologic
and biochemical markers for such intermediate transitional cells; third,
study the regulation of this Leydig cell developmental process both in situ
and in vitro.  In the adult rat, we propose studies designed to:  first,
elucidate the "trophic" effect of LH on Leydig cell division, number and
intratesticular mitogenic activity and transforming growth factor beta
content; and second, test the effect of LH on Leydig cell peroxisome
structure and function.

## Key facts

- **NIH application ID:** 2195241
- **Project number:** 5R01HD007204-22
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **SAM.gov UEI:** FTMTDMBR29C7
- **Principal Investigator:** BARRY R ZIRKIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $250,691
- **Award type:** 5
- **Project period:** 1978-02-01 → 1995-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2195241

## Citation

> US National Institutes of Health, RePORTER application 2195241, REGULATION OF ANDROGEN SECRETION IN MAMMALIAN TESTES (5R01HD007204-22). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2195241. Licensed CC0.

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