The Effect of Glucocorticoids on Estrogen-Dependent Luteinizing Hormone Release in the Ovariectomized Rat and on Gonadotropin Secretion in the Intact Female Rat*

Baldwin, David M.

doi:10.1210/endo-105-1-120

Cited by 111 publications

(56 citation statements)

References 37 publications

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“…In the present study, ACTH treatment reduced the weights of the fetus and placenta (Table 1), which confirmed the previous report for mice (Paul & D'Angelo, 1972). There are several reports that adrenalectomy or corticoid treatment of the mother affect fetal adrenal function (Knobil & Briggs, 1954;Baldwin, 1979). Although Ochiai et al (1983) (Fig.…”

Section: Introductionsupporting

confidence: 92%

Inhibitory effects of adrenocorticotrophin or corticosterone on progesterone secretion during mid-pregnancy in rats

Katô

Nanjo²,

Numa³

et al. 1988

Reproduction

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Section: Introductionsupporting

confidence: 92%

Inhibitory effects of adrenocorticotrophin or corticosterone on progesterone secretion during mid-pregnancy in rats

Katô

Nanjo²,

Numa³

et al. 1988

Reproduction

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“…Increased glucocorticoid levels disrupt and suppress endocrine signaling in the male reproductive axis. Elevations in circulating corticosteroid after stresses result in a significant drop in testosterone secretion [6,7]. A similar pattern is observed in rats subjected to restrained stress [8][9][10][11].…”

Section: Stress and Leydig Cell Functionsupporting

confidence: 56%

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Lian

Lin

et al. 2008

Steroids

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Stress-mediated elevations in circulating glucocorticoid levels lead to corresponding rapid declines in testosterone production by Leydig cells in the testis. In previous studies we have established that glucocorticoids act on Leydig cells directly, through the classic glucocorticoid receptor (GR), and that access to the GR is controlled prior to the GR by a metabolizing pathway mediated by the type 1 isoform of 11β-hydroxysteroid dehydrogenase (11βHSD1). This enzyme is bidirectional (with both oxidase and reductase activities) and in the rat testis is exclusively localized in Leydig cells where it is abundantly expressed and may catalyze the oxidative inactivation of glucocorticoids. The predominant reductase direction of 11βHSD1 activity in liver cells is determined by an enzyme, hexose-6-phosphate dehydrogenase (H6PDH), on the luminal side of the smooth endoplasmic reticulum (SER). Generation of the pyridine nucleotide cofactor NADPH by H6PDH stimulates the reductase direction of 11βHSD1 resulting in increased levels of active glucocorticoids in liver cells. Unlike liver cells, steroidogenic enzymes including 17β-hydroxysteroid dehydrogenase 3 (17βHSD3) forms the coupling with 11βHSD1. Thus the physiological concentrations of androstenedione serve as a substrate for 17βHSD3 utilizing NADPH to generate NADP+, which drives 11βHSD1 in Leydig cells primarily as an oxidase; thus eliminating the adverse effects of glucocorticoids on testosterone production. At the same time 11βHSD1 generates NADPH which promotes testosterone biosynthesis by stimulating 17βHSD3 in a cooperative cycle. This enzymatic coupling constitutes a rapid mechanism for modulating glucocorticoid control of testosterone biosynthesis. Under stress conditions, glucocorticoids also have rapid actions to suppress cAMP formation thus to lower testosterone production.

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“…X70. trous cycle, were also consistent with effects described for synthetic glucocorticosteroids in the dog (23). Inhibition of ovulation due to glucocorticosteroid-induced suppression of luteinizing hormone (LH) release (ie, preovulatory LH surge) has been described for rodents and women (4,12,13,38). Inhibition of the preovulatory LH surge in female rabbits has also been demonstrated with medroxyprogesterone acetate (31).…”

Section: Methodssupporting

confidence: 76%

Chronic Effects of the Novel Glucocorticosteroid RPR 106541 Administered to Beagle Dogs by Inhalation

Miller¹,

Valerio²,

Pino³

et al. 2000

Toxicol Pathol

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The Effect of Glucocorticoids on Estrogen-Dependent Luteinizing Hormone Release in the Ovariectomized Rat and on Gonadotropin Secretion in the Intact Female Rat*

Cited by 111 publications

References 37 publications

Inhibitory effects of adrenocorticotrophin or corticosterone on progesterone secretion during mid-pregnancy in rats

Inhibitory effects of adrenocorticotrophin or corticosterone on progesterone secretion during mid-pregnancy in rats

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Chronic Effects of the Novel Glucocorticosteroid RPR 106541 Administered to Beagle Dogs by Inhalation

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