LH RECEPTORS AND STEROIDOGENESIS IN DISTINCT POPULATIONS OF LEYDIG CELLS *

Luteinizing hormone (LH) has been shown to be the only hormone essential for maintenance of testicular testosterone pr0duction.l LH mediates its effect on testicular steroidogenesis by binding to high affinity receptors in the plasma membrane of Leydig cells. In recent years, numerous investigators have reported that in vivo administration of LH or human chorionic gonadotropin (hCG) results in the reduction of the number of testicular LH receptors1-’ accompanied by a decrease in testosterone production 4, 6+ in response to subsequent stimulation by LH or hCG. Studies from our laboratory, however, have demonstrated that changes in LH receptor number may be dissociated from changes in LH-stimulated testosterone production following in vivo treatment with gonadotropins.1 We observed that only a single high dose of LH, 100 pg or greater, caused a decrease in testicular responsiveness, whereas twice daily injections of LH for six days or longer were accompanied by a time-related increase in in vivo testicular testosterone secretion in response to a subsequent stimulatory dose of LH. The LH-induced loss of testicular LH receptors was similar in rats that received a single high dose of LH and in rats that received twice daily injections. These observations indicate that different modes of in vivo LH treatment have markedly different effects on testicular responsiveness to subsequent LH/hCG stimulation. Interpretation of these results, however, is complicated by the possibility that chronic pituitary hormone treatment may change ( 1 ) sensitivity of the Leydig cells to subsequent LH stimulation, ( 2 ) secretion or clearance rate of testosterone, and/or ( 3 ) total number of Leydig cells. To distinguish among these possibilities, changes in Leydig cell LH receptor concentration and responsiveness to LH were assessed in the same cells after different modes of in vivo hormone treatment. Using Metrizamide gradient centrifugation to separate dispersed testicular cells, we found evidence for two distinct populations of Leydig cells.* Leydig cells of these two populations contain similar numbers of LH receptor sites but exhibit marked differences in testosterone production in response to in vitro

[1]  P. O’Shaughnessy,et al.  Differential steroidogenic enzyme activities in different populations of rat Leydig cells. , 1981, Endocrinology.

[2]  K. Catt,et al.  Estradiol receptor-mediated regulation of steroidogenesis in gonadotropin-desensitized Leydig cells. , 1981, The Journal of biological chemistry.

[3]  A. Payne,et al.  Differential effects of single and repeated administrations of gonadotropins on luteinizing hormone receptors and testosterone synthesis in two populations of Leydig cells. , 1980, The Journal of biological chemistry.

[4]  J. Downing,et al.  Luteinizing hormone receptors and testosterone synthesis in two distinct populations of Leydig cells. , 1980, Endocrinology.

[5]  K. Catt,et al.  Estrogen dependence of a gonadotropin-induced steroidogenic lesion in rat testicular Leydig cells. , 1980, The Journal of clinical investigation.

[6]  B. Zirkin,et al.  Testosterone secretion by rat, rabbit, guinea pig, dog, and hamster testes perfused in vitro: correlation with Leydig cell ultrastructure. , 1980, Endocrinology.

[7]  B. Zirkin,et al.  Testosterone secretion by rat, rabbit, guinea pig, dog, and hamster testes perfused in vitro: correlation with Leydig cell mass. , 1979, Endocrinology.

[8]  L. Valladares,et al.  Acute stimulation of aromatization in Leydig cells by human chorionic gonadotropin in vitro. , 1979, Proceedings of the National Academy of Sciences of the United States of America.

[9]  L. Valladares,et al.  Induction of testicular aromatization by luteinizing hormone in mature rats. , 1979, Endocrinology.

[10]  A. Payne,et al.  Synergistic Effect of Follicle-Stimulating Hormone and Luteinizing Hormone on Testicular δ-3β-Hydroxysteroid Dehydrogenase-isomerase: Application of a New Method for the Separation of Testicular Compartments , 1979 .

[11]  J. Canick,et al.  Testicular aromatization in immature rats: localization and stimulation after gonadotropin administration in vivo. , 1979, Endocrinology.

[12]  R. Kelch,et al.  Dissociation of lutropin-induced loss of testicular lutropin receptors and lutropin-induced desensitization of testosterone synthesis. , 1978, Biochimica et biophysica acta.

[13]  F. Haour,et al.  Early hCG-induced desensitization in Leydig cells. , 1978, Biochemical and biophysical research communications.

[14]  D. Armstrong,et al.  Control of testicular estrogen synthesis. , 1978, Biology of reproduction.

[15]  K. Catt,et al.  Hormonal regulation of testicular luteinizing hormone receptors. Effects on cyclic AMP and testosterone responses in isolated Leydig cells. , 1977, The Journal of biological chemistry.

[16]  P. Torjesen,et al.  hCG suppression of LH receptors and responsiveness of testicular tissue to hCG , 1977, Molecular and Cellular Endocrinology.

[17]  K. Catt,et al.  Gonadotropin-induced regulation of luteinizing hormone receptors and desensitization of testicular 3':5'-cyclic AMP and testosterone responses. , 1977, Proceedings of the National Academy of Sciences of the United States of America.

[18]  R. Kelch,et al.  Hypothalamic, pituitary and testicular function during sexual maturation of the male rat. , 1977, The Journal of endocrinology.

[19]  R. Sharpe.  hCG-induced decrease in availability of rat testis receptors , 1976, Nature.

[20]  E. Murono,et al.  Distinct testicular 17-ketosteroid reductases, one in interstitial tissue and one in seminiferous tubules. Differential modulation by testosterone and metabolites of testosterone. , 1976, Biochimica et biophysica acta.

[21]  K. Catt,et al.  Regulation of luteinizing hormone receptors in testicular interstitial cells by gonadotropin. , 1976, Biochemical and biophysical research communications.

[22]  W. Neaves.  Leydig cells. , 1975, Contraception.

[23]  A. Goldman,et al.  Developmental defects of testicular morphology and steroidogenesis in the male rat pseudohermaphrodite and response to testosterone and dihydrotestosterone. , 1974, Endocrinology.