State of rat adrenal glucocorticoid function in pinealectomy

1987 ◽  
Vol 17 (5) ◽  
pp. 446-448
Author(s):  
V. A. Kosykh ◽  
T. V. Lasukova ◽  
Yu. G. Kozlova
1998 ◽  
Vol 104 (1) ◽  
pp. 61-71 ◽  
Author(s):  
Stefan Hasinski

2019 ◽  
Vol 20 (8) ◽  
pp. 627-640 ◽  
Author(s):  
Truong San Phan ◽  
Verena M. Merk ◽  
Thomas Brunner

Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 69-72 ◽  
Author(s):  
A Munck ◽  
PM Guyre

What are the normal functions of the adrenal glucocorticoid hormones? This seemingly simple question has not yet any simple agreed-on answer. In the half-century since the glucocorticoids were distinguished from other cortical steroids, the question of their physiological functions has generated much inconclusive debate. Likewise, questions of their role in disease and therapy lack definitive answers. The authors propose that there is no fundamental distinction between the physiological and pharmacological effects of glucocorticoids and that their inhibitory actions on inflammatory and immune responses are concerned with modulating the body's defense mechanisms.


2004 ◽  
Vol 32 (2) ◽  
pp. 557-569 ◽  
Author(s):  
F Gizard ◽  
E Teissier ◽  
I Dufort ◽  
G Luc ◽  
V Luu-The ◽  
...  

Steroid hormones synthesized from cholesterol in the adrenal gland are important regulators of many physiological processes. It is now well documented that the expression of many genes required for steroid biosynthesis is dependent on the coordinated expression of the nuclear receptor steroidogenic factor-1 (SF-1). However, transcriptional mechanisms underlying the species-specific, developmentally programmed and hormone-dependent modulation of the adrenal steroid pathways remain to be elucidated. Recently, we demonstrated that the transcriptional regulating protein of 132 kDa (TReP-132) acts as a coactivator of SF-1 to regulate human P450scc gene transcription in human adrenal NCI-H295 cells. The present study shows that overexpression of TReP-132 increases the level of active steroids produced in NCI-H295 cells. The conversion of pregnenolone to downstream steroids following TReP-132 expression showed increased levels of glucocorticoids, C(19) steroids and estrogens. Correlating with these data, TReP-132 increases P450c17 activities via the induction of transcript levels and promoter activity of the P450c17 gene, an effect that is enhanced in the presence of cAMP or SF-1. In addition, P450aro activity and mRNA levels are highly induced by TReP-132, whereas 3beta-hydroxysteroid dehydrogenase type II and P450c11aldo transcript levels are only slightly modulated. Taken together, these results demonstrate that TReP-132 is a trans-acting factor of genes involved in adrenal glucocorticoid, C(19) steroid and estrogen production.


Life Sciences ◽  
1998 ◽  
Vol 62 (19) ◽  
pp. 1783-1787 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Giuseppe Gottardo ◽  
Gastone G. Nussdorfer

Author(s):  
Jaruwan Khonmee ◽  
◽  
Jureerat Sumretprasong ◽  
Janine L. Brown ◽  
Kamraitip Lokham ◽  
...  

2019 ◽  
Vol 45 (1) ◽  
pp. 34-37
Author(s):  
A. D. Dobracheva ◽  
N. P. Goncharov ◽  
T. N. Todua ◽  
I. D. Nizharadze

Relationships between secretion of pituitary gonadotropic hormones, adrenal glucocorticoid and androgenic function, and ovarian steroid production were studied in 14 patients with the polycystic ovaries syndrome (POS) under conditions of suppressed endogenous gonadotropic secretion, which was induced by tonic administration of busereline, a GnRH agonist. The bRH/iRH ratio is not changed in POS patients under conditions of suppressed gonadotropic secretion. Inhibition of gonadotropic secretion leads to decrease of estrogen secretion in the ovaries and does not affect the adrenal glucocorticoid function. Activation of adrenal androgen production by the delta-5 pathway was observed in 57% patients under conditions of gonadotroph inhibition. Three months after busereline was discontinued, adrenal steroidogenesis normalized. The results permit a conclusion that prolonged inhibition of gonadotropic secretion with GnRH agonist does not change the bLH/iLH ratio but can lead to activation of adrenal androgen production in part of patients with POS.


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