scholarly journals Glucocorticoid production in the thymus and brain: immunosteroids and neurosteroids

2021 ◽  
pp. 100352
Author(s):  
Melody Salehzadeh ◽  
Kiran K. Soma
Keyword(s):  
Glucocorticoid Production

Gonadotrophin-secretion in adrenocortical insufficiency: impact of glucocorticoid substitution

1982 ◽  
Vol 101 (4) ◽  
pp. 580-585 ◽  
Author(s):  
H. Vierhapper ◽  
W. Waldhäusl ◽  
P. Nowotny
Keyword(s):  
Adrenal Insufficiency ◽  
Secretory Response ◽  
Bilateral Adrenalectomy ◽  
Substitution Therapy ◽  
Adrenocortical Insufficiency ◽  
Primary Adrenal Insufficiency ◽  
Gonadotrophin Secretion ◽  
Glucocorticoid Production

Abstract. In patients with deficient endogenous glucocorticoid production due to primary adrenal insufficiency (n = 4) or bilateral adrenalectomy (n = 2) a rise in LRH-stimulated concentrations of LH was seen following withdrawal of substitution therapy for 84 h. Consecutive re-administration of glucocorticoids (dexamethasone 2.0 mg/day for 3 days) resulted in increased basal concentrations of LH and FSH and a diminished secretory response of LH upon iv LRH (100 μg). Five patients substituted with glucocorticoids because of adrenocortical insufficiency presented upon the administration of exogenous ACTH1-24 with unchanged basal and LRH-stimulated concentrations of LH and FSH as compared to a placebo experiment. These data suggest that the withdrawal and subsequent re-administration of glucocorticoid substitution alters basal and stimulated concentrations of gonadotrophins in patients with adrenocortical insufficiency, thus providing evidence for the importance of adequate glucocorticoid supply in the regulation of gonadotrophin secretion.

scholarly journals Glucocorticoid production in the chicken bursa and thymus

2001 ◽  
Vol 13 (6) ◽  
pp. 769-776 ◽  
Author(s):  
Oskar Lechner ◽  
Hermann Dietrich ◽  
G. Jan Wiegers ◽  
Melanie Vacchio ◽  
Georg Wick
Keyword(s):  
Glucocorticoid Production

Glucocorticoid Production, Activity Levels, And Personality Traits Of Fennec Foxes (Vulpes zerda) Managed For Different Roles In Zoos

2021 ◽  
pp. 1-18
Author(s):  
Corinne P. Kozlowski ◽  
Karen L. Bauman ◽  
Ashley D. Franklin ◽  
John M. Sahrmann ◽  
Marieke Gartner ◽  
...  
Keyword(s):  
Personality Traits ◽  
Activity Levels ◽  
Production Activity ◽  
Glucocorticoid Production

scholarly journals The Pituitary Function of Androgen Receptor Constitutes a Glucocorticoid Production Circuit

2007 ◽  
Vol 27 (13) ◽  
pp. 4807-4814 ◽  
Author(s):  
Junko Miyamoto ◽  
Takahiro Matsumoto ◽  
Hiroko Shiina ◽  
Kazuki Inoue ◽  
Ichiro Takada ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Negative Feedback ◽  
Late Onset ◽  
Feedback Regulation ◽  
Feedback System ◽  
Cell Types ◽  
Positive Control ◽  
Negative Feedback Regulation ◽  
Pituitary Glands ◽  
Glucocorticoid Production

ABSTRACT Androgen receptor (AR) mediates diverse androgen actions, particularly reproductive processes in males and females. AR-mediated androgen signaling is considered to also control metabolic processes; however, the molecular basis remains elusive. In the present study, we explored the molecular mechanism of late-onset obesity in male AR null mutant (ARKO) mice. We determined that the obesity was caused by a hypercorticoid state. The negative feedback system regulating glucocorticoid production was impaired in ARKO mice. Male and female ARKO mice exhibited hypertrophic adrenal glands and glucocorticoid overproduction, presumably due to high levels of adrenal corticotropic hormone. The pituitary glands of the ARKO males had increased expression of proopiomelanocortin and decreased expression of the glucocorticoid receptor (GR). There were no overt structural abnormalities and no alteration in the distribution of cell types in the pituitaries of male ARKO mice. Additionally, there was normal production of the other hormones within the glucocorticoid feedback system in both the pituitary and hypothalamus. In a cell line derived from pituitary glands, GR expression was under the positive control of the activated AR. Thus, this study suggests that the activated AR supports the negative feedback regulation of glucocorticoid production via up-regulation of GR expression in the pituitary gland.

Local glucocorticoid production in the thymus

Steroids ◽  
2015 ◽  
Vol 103 ◽  
pp. 58-63 ◽  
Author(s):  
Gergely Talaber ◽  
Mikael Jondal ◽  
Sam Okret
Keyword(s):  
Glucocorticoid Production

EFFECT OF METOPIRONE IN A PATIENT WITH ADRENAL CORTICAL CARCINOMA

1963 ◽  
Vol 44 (3) ◽  
pp. 346-354 ◽  
Author(s):  
H. Daniels ◽  
W. J. van Amstel ◽  
W. Schopman ◽  
C. van Dommelen
Keyword(s):  
Cushing’S Syndrome ◽  
Clinical Effect ◽  
Cushing's Syndrome ◽  
Adrenal Cortical Carcinoma ◽  
List Type ◽  
Adrenal Carcinoma ◽  
Glucocorticoid Production ◽  
Steroid Excretion

ABSTRACT The effect of metopirone® (SU-4885)* in a patient with metastatic adrenal cortical carcinoma was studied. The intention was to depress the symptoms of Cushing's syndrome, due to a high glucocorticoid production by the carcinoma. The excretion of 17-KS, 17-KGS, 11-oxo(y)-17-OHCS and 11-desoxy-17-OHCS was followed for seven weeks. The steroid excretion was variable. The 11-oxo(y)-17-OHCS showed a significant decrease during treatment with SU-4885 for seven weeks. The ratio 11-oxo(y)-17-OHCS: 11-desoxy-17-OHCS fell from 1.7 to 0.1 during this period. The excessive glucocorticoid production of the metastatic adrenal carcinoma was suppressed as long as treatment continued. It was not possible to judge the clinical effect of SU-4885 because of the progressive nature of the disease.

scholarly journals Transgenic overexpression of hexose-6-phosphate dehydrogenase in adipose tissue causes local glucocorticoid amplification and lipolysis in male mice

2014 ◽  
Vol 306 (5) ◽  
pp. E543-E551 ◽  
Author(s):  
Ying Wang ◽  
Limei Liu ◽  
Hanze Du ◽  
Yoshiko Nagaoka ◽  
Winnie Fan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Visceral Obesity ◽  
Abdominal Fat ◽  
Fatty Acid Binding ◽  
Metabolic Phenotypes ◽  
Lipolytic Action ◽  
Glucocorticoid Production

The prereceptor activation of glucocorticoid production in adipose tissue by NADPH-dependent 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) has emerged as a potential mechanism in the pathogenesis of visceral obesity and metabolic syndrome. Hexose-6-phosphate dehydrogenase (H6PDH) is an endoplasmic reticulum lumen-resident enzyme that generates cofactor NADPH and thus mediates 11β-HSD1 activity. To determine the role of adipose H6PDH in the prereceptor modulation of 11β-HSD1 and metabolic phenotypes, we generated a transgenic (Tg) mouse model overexpressing H6PDH under the control of the enhancer-promoter region of the adipocyte fatty acid-binding protein (aP2) gene (aP2/H6PDH Tg mice). Transgenic aP2/H6PDH mice exhibited relatively high expression of H6PDH and elevated corticosterone production with induction of 11β-HSD1 activity in adipose tissue. This increase in corticosterone production in aP2-H6PDH Tg mice resulted in mild abdominal fat accumulation with induction of C/EBP mRNA expression and slight weight gain. Transgenic aP2/H6PDH mice also exhibited fasting hyperglycemia and glucose intolerance with insulin resistance. In addition, the aP2/H6PDH Tg mice have elevated circulating free fatty acid levels with a concomitant increased adipose lipolytic action associated with elevated HSL mRNA and Ser660 HSL phosphorylation within abdominal fat. These results suggest that increased H6PDH expression specifically in adipose tissue is sufficient to cause intra-adipose glucocorticoid production and adverse metabolic phenotypes. These findings suggest that the aP2/H6PDH Tg mice may provide a favorable model for studying the potential impact of H6PDH in the pathogenesis of human metabolic syndrome.

scholarly journals p54nrb/NONO Regulates Cyclic AMP-Dependent Glucocorticoid Production by Modulating Phosphodiesterase mRNA Splicing and Degradation

2015 ◽  
Vol 35 (7) ◽  
pp. 1223-1237 ◽  
Author(s):  
Jia Yang Lu ◽  
Marion B. Sewer
Keyword(s):  
Cyclic Amp ◽  
Nuclear Protein ◽  
Intracellular Camp ◽  
Acth Stimulation ◽  
Content Type ◽  
Control Gene Expression ◽  
Rna Export ◽  
The Stability ◽  
Glucocorticoid Production ◽  
Nuclear Processes

Glucocorticoid production in the adrenal cortex is activated in response to an increase in cyclic AMP (cAMP) signaling. The nuclear protein p54nrb/NONO belongs to theDrosophilabehavior/human splicing (DBHS) family and has been implicated in several nuclear processes, including transcription, splicing, and RNA export. We previously identified p54nrb/NONO as a component of a protein complex that regulates the transcription of CYP17A1, a gene required for glucocorticoid production. Based on the multiple mechanisms by which p54nrb/NONO has been shown to control gene expression and the ability of the protein to be recruited to the CYP17A1 promoter, we sought to further define the molecular mechanism by which p54nrb/NONO confers optimal cortisol production. We show here that silencing p54nrb/NONO expression in H295R human adrenocortical cells decreases the ability of the cells to increase intracellular cAMP production and subsequent cortisol biosynthesis in response to adrenocorticotropin hormone (ACTH) stimulation. Interestingly, the expression of multiple phosphodiesterase (PDE) isoforms, including PDE2A, PDE3A, PDE3B, PDE4A, PDE4D, and PDE11A, was induced in p54nrb/NONO knockdown cells. Investigation of the mechanism by which silencing of p54nrb/NONO led to increased expression of select PDE isoforms revealed that p54nrb/NONO regulates the splicing of a subset of PDE isoforms. Importantly, we also identify a role for p54nrb/NONO in regulating the stability of PDE transcripts by facilitating the interaction between the exoribonuclease XRN2 and select PDE transcripts. In summary, we report that p54nrb/NONO modulates cAMP-dependent signaling, and ultimately cAMP-stimulated glucocorticoid biosynthesis by regulating the splicing and degradation of PDE transcripts.

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