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Research Article Free access | 10.1172/JCI109716

Estrogen Dependence of a Gonadotropin-induced Steroidogenic Lesion in Rat Testicular Leydig Cells

S. B. Cicorraga, S. Sorrell, J. Bator, K. J. Catt, and M. L. Dufau

Section on Molecular Endocrinology and Hormonal Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Section on Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Find articles by Cicorraga, S. in: PubMed | Google Scholar

Section on Molecular Endocrinology and Hormonal Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Section on Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Find articles by Sorrell, S. in: PubMed | Google Scholar

Section on Molecular Endocrinology and Hormonal Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Section on Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Find articles by Bator, J. in: PubMed | Google Scholar

Section on Molecular Endocrinology and Hormonal Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Section on Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Find articles by Catt, K. in: PubMed | Google Scholar

Section on Molecular Endocrinology and Hormonal Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Section on Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20205

Find articles by Dufau, M. in: PubMed | Google Scholar

Published March 1, 1980 - More info

Published in Volume 65, Issue 3 on March 1, 1980
J Clin Invest. 1980;65(3):699–705. https://doi.org/10.1172/JCI109716.
© 1980 The American Society for Clinical Investigation
Published March 1, 1980 - Version history
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Abstract

Leydig cells isolated from the testes of rats treated with intravenous exogenous gonadotropin (hCG) or subcutaneous gonadotropin-releasing hormone (GnRH) show markedly decreased luteinizing hormone (LH) receptors and a partial block in testicular 17,20 desmolase activity. In contrast, Leydig cells from animals with equivalent degrees of LH receptor loss induced by subcutaneous hCG treatment show no change in 17,20 desmolase activity. These findings indicated that the acuteness of gonadotrophic stimulation, rather than the extent of LH receptor loss, was responsible for the steroidogenic lesion. A role of estradiol in the enzymatic block produced in vivo by acute elevation of circulating gonadotropin (intravenous hCG or GnRH-stimulated endogenous LH) was suggested by rapid elevations of testicular 17β-estradiol within 30 min after intravenous hCG, whereas more gradual increases in estradiol occurred 4-8 h after subcutaneous hCG. The inhibitory effect of endogenous estrogen on testicular steroidogenesis was confirmed by the ability of an estrogen antagonist (Tamoxifen) to prevent the reduction of testosterone responses caused by intravenous hCG and subcutaneous GnRH. In addition, Tamoxifen significantly increased the number of LH receptors in Leydig cells from both control and gonadotropin-desensitized animals. These findings indicate that the acute elevations of intratesticular estrogen produced by treatment with hCG or GnRH are responsible for the steroidogenic lesion seen in gonadotropin-desensitized Leydig cells. These results also suggest that locally produced estrogens contribute to the regulation of testicular LH receptors and 17,20 desmolase activity.

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