Regulation by dexamethasone of the 3β-hydroxysteroid dehydrogenase activity in adult rat leydig cells

Agular, Birte-Marie; Vinggaard, Anne Marie; Vind, Constance

doi:10.1016/0960-0760(92)90245-e

Cited by 34 publications

(13 citation statements)

References 34 publications

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“…In this context, it is worth mentioning that dexamethasone blocked the ACTH-induced decrease of the plasma testosterone concentration (Table 1), and that dexamethasone pretreatment neither reduced the LH plasma concentrations (Table 1) nor affected the human chorionic gonadotropin (hCG)-induced increment in the plasma testosterone of guinea pigs (data not shown). These findings disagree with previous results which demonstrated: (1) a drop of testosterone plasma levels after dexamethasone injection (Saez et al 1977, Chantaraprateep & Thibier 1978, Kim et al 1985, (2) a decreased in vivo response of the testes to luteinizing hormone-releasing hormone (LHRH)/LH (Chantaraprateep & Thibier 1978) or to hCG (Saez et al 1977) after dexamethasone pretreatment, (3) a dexamethasone-dependent reduction of basal testosterone secretion by cultured Leydig cells (Saez et al 1977, Agular et al 1992, Monder et al 1992, 1994b, and (4) a dexamethasone-induced suppression of the hCGstimulated testosterone secretion in vitro (Bambino & Hsueh 1981, Welsh et al 1982, Agular et al 1992, Orr & Mann 1992.…”

Section: Discussioncontrasting

confidence: 93%

Role of cortisol in the ACTH-induced suppression of testicular steroidogenesis in guinea pigs

Fenske

1997

Journal of Endocrinology

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In order to investigate the role of cortisol in the regulation of testicular function, adult male guinea pigs were challenged with ACTH (20 IU), cortisol (8 or 16 mumol), or with ACTH plus dexamethasone (DEX, 2 mumol). The amounts of cortisol, testosterone, progesterone, and androstenedione present in the plasma or secreted by incubated adrenals or testes were determined by radioimmunoassay. The plasma concentrations of LH were determined using a radioimmunoassay for rat LH. ACTH treatment elevated cortisol plasma concentrations to 999% of control values, whereas it reduced testosterone plasma levels to 43% of control values. ACTH treatment did not affect LH plasma levels. A significant negative correlation was found in ACTH-treated animals, when the cortisol and testosterone plasma concentrations in serially taken blood samples (30-240 min after treatment) were compared (rs = -0.90 and rs = -0.99, P < 0.05). In addition to cortisol, ACTH raised progesterone and androstenedione plasma concentrations. If animals were treated with 2 mumol DEX + ACTH, the plasma levels of cortisol and androstenedione but not of progesterone, testosterone or LH were changed. ACTH stimulated the in vitro secretion of cortisol, progesterone and androstenedione by the adrenals but reduced the in vitro release of androstenedione and testosterone by the testes. In summary, treatment of guinea pigs resulted in elevated cortisol and in reduced testosterone plasma concentrations. The mechanism of the cortisol-induced inhibition of testicular function was independent of the LH plasma concentrations. The in vitro experiments indicate that cortisol directly interacts with the Leydig cells, presumably by inhibiting the activity of the testicular 17 alpha-hydroxylase and/or C17,20-lyase. Taking into account the results of comparable investigations in the rat, the inhibition of the testicular 17 alpha-hydroxylase and/or C17,20-lyase takes place if the intracellular cortisol exceeds the capacity of the 11 beta-hydroxysteroid dehydrogenase to inactivate it.

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Section: Discussioncontrasting

confidence: 93%

Role of cortisol in the ACTH-induced suppression of testicular steroidogenesis in guinea pigs

Fenske

1997

Journal of Endocrinology

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“…Administration of PRL to hypophysectomised rats also stimulated testicular 30-HSD activity (Halle/ et al, 1971). On the contrary, dexamethasone inhibited immature and adult rat Ley-dig cellular 30-HSD activity in vitro (Agular et al, 1992;Agular and Vind, 1995). Earlier studies reveal an increase in plasma corticosteroid (Rhees et al, 1983) and a decrease in plasma IGF-I (Olchovsky et al, 1990) in alloxan/STZ-diabetic rats.…”

Section: Discussionmentioning

confidence: 89%

Influence of streptozotocin-induced diabetes and insulin treatment on the pituitarv-testicular axis during sexual maturation in rats

Murthy¹,

Valli²,

Pm³

et al. 2012

Exp Clin Endocrinol Diabetes

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Effects of streptozotocin (STZ) diabetes and insulin treatment on the functioning of pituitary-testicular axis during sex ual maturation was studied. Prepubertal (30 days old) and pubertal (50 days old) male Wistar rats were made diabetic by a single injec tion of STZ. A group of diabetic rats was given insulin (3U/100 g b.wt./day in 2 equally divided doses), 3 days after STZ treatment. Prepubertal and pubertal rats of all groups were killed on postnatal days 51 and 71, respectively. STZ-diabetes caused marked reduction in serum EH, ESH, prolactin, testosterone and testicular interstitial tluid testosterone as well as the activities of Leydig cellular ster oidogenic enzymes (3[i-and 17P-hydroxysteroid dehydrogenases). Insulin treatment to diabetic rats maintained these changes at con trol range except FSH and prolactin in prepubertal rats. The results indicate that (i) diabetes-induced steroidogenic lesions in l.eydig cells represent a direct consequence of dysfunctioning of pituitarytesticular axis, (ii) the adverse effects of diabetes on pituitarytesticular functions are influenced by age of its induction and (iii) optimum insulin level is essential for the acquisition of Eeydig cellular steroidogenic efficacy during sexual development.

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“…c p b 0.01 compared with control/NC. mechanisms of steroidogenic inhibition in Leydig cells by glucocorticoids during stress include the inhibition of the transcription of genes encoding testosterone biosynthetic enzymes (Orr et al, 1994), as well as the reduction in steroidogenic enzyme level, including 20-22 lyase, 3β-hydroxysteroid dehydrogenase, and 17α-hydroxylase/C17-20 lyase (Payne and Youngblood, 1995;Aguilar et al, 1992;Orr and Mann, 1990). The extent of glucocorticoid activity in Leydig cells depends on whether the steroid is metabolized or not.…”

Section: Discussionmentioning

confidence: 98%

Sexual behavior attenuates the effects of chronic stress in body weight, testes, sexual accessory glands, and plasma testosterone in male rats

Retana‐Márquez

Vigueras-Villaseñor

Juárez‐Rojas

et al. 2014

Hormones and Behavior

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Regulation by dexamethasone of the 3β-hydroxysteroid dehydrogenase activity in adult rat leydig cells

Cited by 34 publications

References 34 publications

Role of cortisol in the ACTH-induced suppression of testicular steroidogenesis in guinea pigs

Role of cortisol in the ACTH-induced suppression of testicular steroidogenesis in guinea pigs

Influence of streptozotocin-induced diabetes and insulin treatment on the pituitarv-testicular axis during sexual maturation in rats

Sexual behavior attenuates the effects of chronic stress in body weight, testes, sexual accessory glands, and plasma testosterone in male rats

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