T
Thomas H. Bambino
Researcher at University of California, San Diego
Publications - 5
Citations - 711
Thomas H. Bambino is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Testosterone & Human chorionic gonadotropin. The author has an hindex of 4, co-authored 5 publications receiving 695 citations.
Papers
More filters
Journal ArticleDOI
Direct inhibitory effect of glucocorticoids upon testicular luteinizing hormone receptor and steroidogenesis in vivo and in vitro.
TL;DR: The direct inhibitory effect of glucocorticoids on testicular LH receptor content and steroidogenesis is demonstrated, suggesting the adrenal glucocORTicoids may regulate testis functions.
Journal ArticleDOI
Mechanism of glucocorticoid-induced suppression of testicular androgen biosynthesis in vitro.
TL;DR: It is suggested that glucocorticoids directly suppress Leydig cell steroidogenesis by decreasing gonadotropin stimulation of cAMP production and the activity of 17 alpha-hydroxylase.
Journal ArticleDOI
Gonadotropin-releasing hormone and its agonist inhibit testicular luteinizing hormone receptor and steroidogenesis in immature and adult hypophysectomized rats
TL;DR: In vitro studies demonstrated that treatment with the GnRH agonist in vivo inhibited both basal and hCG-stimulated androgen production in FSH-primed immature hypophysectomized rats and inhibited in vitro testicular steroidogenic responses in adult hypopysectomization rats.
Journal ArticleDOI
Mechanism of the Direct Action of Gonadotropin-Releasing Hormone and Its Antagonist on Androgen Biosynthesis by Cultured Rat Testicular Cells*
TL;DR: The present results demonstrate that GnRH and its analogs exert direct actions on testicular cells through stereospecific recognition sites and occur at sites distal to the formation of cAMP and pregnenolone and may be due to decreases in the activity of the enzymes 17 alpha-hydroxylase and 17-20 desmolase.
of Testicular Androgen Biosynthesis In Vitro
TL;DR: The results suggest that glucocorticoids directly suppress Leydig cell steroidogenesis by decreasing gonadotropin stimulation of cAMP production and the activity of 17o-hydroxylase.