scholarly journals Embryonic osteocalcin signalling determines lifelong adrenal steroidogenesis and homeostasis in the mouse

2021 ◽  
Author(s):  
Vijay K. Yadav ◽  
Julian M. Berger ◽  
Parminder Singh ◽  
Perumal Nagarajan ◽  
Gerard Karsenty
Keyword(s):  
Adrenal Steroidogenesis

EARLY VARIATIONS OF PLASMA CORTISOL AFTER PULSE INTRAVENOUS INJECTION OF DIBUTYRYL CYCLIC ADENOSINE 3′,5′-MONOPHOSPHATE IN NORMAL SUBJECTS

1973 ◽  
Vol 72 (4) ◽  
pp. 753-761 ◽  
Author(s):  
Alberto Angeli ◽  
Giuseppe Boccuzzi ◽  
Roberto Frajria ◽  
Daniela Bisbocci ◽  
Franco Ceresa
Keyword(s):  
Intravenous Injection ◽  
Plasma Cortisol ◽  
Time Course ◽  
Healthy Adult ◽  
Normal Subjects ◽  
Adult Women ◽  
Healthy Women ◽  
Adrenal Steroidogenesis ◽  
The Mean ◽  
Zero Time

ABSTRACT 10 mg/kg of dibutyryl cyclic adenosine 3′,5′-monophosphate (Db-cAMP) was iv pulse injected into twelve healthy adult women. The plasma cortisol levels were determined as 11-OHCS at zero time and then at 2.5, 5, 7.5, 10, 15, 30, 60 and 180 min after the injection. The data were compared with those obtained at the corresponding times in two groups of eleven and seventeen healthy women after the injection of 250 ng and 250 μg of synthetic β-1-24 corticotrophin performed in the same manner as the injection of the nucleotide. The mean increments in plasma cortisol were significantly lower after Db-cAMP than after ACTH. Differences were noted by analyzing the time course of the responses. In the case of stimulation with Db-cAMP the 11-OHCS levels rose progressively to a maximum at 15–30 min. By contrast, a peak of plasma cortisol was evident in most cases within a few min after the injection of ACTH; after a fall, a later rise was then observed starting from 15 min. The differences in the plasma 11-OHCS responses after the two stimuli may also be of interest clinically for the investigation of some aspects of adrenal steroidogenesis.

Local Regulation of Adrenal Steroidogenesis: Subtle in vitro Effects of IL-1β on the Human Cell Line NCI-H295R Steroid Production along with Changes in MicroRNA Profile and Orphan Nuclear Receptors NR4As

2021 ◽  
pp. 1-11
Author(s):  
Natalia Santucci ◽  
Rocío Stampone ◽  
Eduardo Brandão Ferreira da Silva ◽  
Silvina Villar ◽  
Silvana Spinelli ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Cell Line ◽  
Nuclear Receptors ◽  
Human Cell ◽  
Human Cell Line ◽  
Mirna Profile ◽  
Orphan Nuclear Receptors ◽  
Steroid Production ◽  
Adrenal Steroid ◽  
Adrenal Steroidogenesis

<b><i>Introduction:</i></b> IL-1β, a cytokine from the innate immune response, is well known for its proinflammatory effects and stimulating activity on the hypothalamus-pituitary-adrenal axis, leading to the pituitary synthesis of adrenocorticotropic hormone followed by cortisol (and dehydroepiandrosterone – DHEA) release by the adrenal gland. While IL-1β modulates the adrenal steroidogenesis at the central level, it is unclear whether it also exerts an effect on the adrenal gland. <b><i>Method:</i></b> We studied the effect of IL-1β on adrenal steroid production and steroidogenic enzyme RNA expression in the human cell line NCI-H295R. We also explored eventual changes in the microRNA (miRNA) profile from IL-1β-treated NCI-H295R cells. <b><i>Results:</i></b> Transcripts encoding IL-1β receptors 1 and 2 were noticeable in the cell line, with cortisol and DHEA production showing a subtle increase after cytokine treatment. Transcripts from key enzymes in the steroidogenic pathway were analyzed, with no noticeable changes on them. The miRNA profile was modified by IL-1β treatment to an extent which bears some relationship with the regulatory mechanisms underlying adrenal steroid production. Since orphan nuclear receptors NR4As have emerged as potential key factors for coordinating inflammatory and metabolic responses, cell expression studies were also carried out to show an NR4As transcript augmentation following IL-1β treatment. <b><i>Discussion/Conclusions:</i></b> The subtle increase in adrenal steroid production in response to IL-1β stimulation without any modification in the transcription of the steroidogenic enzymes analyzed suggests an additional inflammatory/anti-inflammatory loop, wherein NR4As receptors may participate. Besides its physiological role, this process might be implied in pathological states accompanied by an unbalanced immune-endocrine relationship.

Inhibition of rat adrenal steroidogenesis by adenine containing compounds

1976 ◽  
Vol 7 (5) ◽  
pp. 401-406
Author(s):  
Seymour B. Koritz ◽  
Abdelrahman M. Moustafa
Keyword(s):  
Adrenal Steroidogenesis

Inhibition of Adrenal Steroidogenesis by Glutethimide

1968 ◽  
Vol 129 (1) ◽  
pp. 20-23 ◽  
Author(s):  
G. G. Johnston ◽  
J. R. Krisle ◽  
R. C. Troop
Keyword(s):  
Adrenal Steroidogenesis

scholarly journals Restoration of adrenal steroidogenesis by adenovirus-mediated transfer of human cytochromeP450 21-hydroxylase into the adrenal gland of21-hydroxylase-deficient mice

Gene Therapy ◽  
1999 ◽  
Vol 6 (11) ◽  
pp. 1898-1903 ◽  
Author(s):  
T Tajima ◽  
T Okada ◽  
X-M Ma ◽  
W J Ramsey ◽  
S R Bornstein ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Adrenal Steroidogenesis ◽  
Deficient Mice

A Case of Congenital Adrenal Hyperplasia due to 3-Beta-Hydroxysteroid Dehydrogenase Deficiency Presented With Acute Liver Failure

2022 ◽  
pp. 097321792110688
Author(s):  
Sarah Alpini ◽  
Rasheda J. Vereen ◽  
Amy Quinn
Keyword(s):  
Liver Failure ◽  
Congenital Adrenal Hyperplasia ◽  
Dehydrogenase Deficiency ◽  
Clinical Presentation ◽  
Hydroxysteroid Dehydrogenase ◽  
Ambiguous Genitalia ◽  
Adrenal Hyperplasia ◽  
Adrenal Steroidogenesis ◽  
Recurrent Hypoglycemia ◽  
Deficiency Cases

Congenital adrenal hyperplasia (CAH) is a group of rare autosomal disorders characterized by a variety of defects in adrenal steroidogenesis. Most cases of CAH are due to an enzyme deficiency in either 21-hydroxylase or 11-beta-hydroxylase. A much rarer form of CAH due to 3-betahydroxysteroid dehydrogenase (3B-HSD) deficiency results in impaired synthesis of all steroid hormones. The clinical presentation of undervirilization in 46 XY patients, hyponatremia, hyperkalemia, and recurrent hypoglycemia in 3B-HSD deficiency cases is well described in the literature. We describe a neonate with 3B-HSD deficiency that presented with ambiguous genitalia and hypoglycemia and was found to have comorbid coagulopathy, cholestasis, and direct hyperbilirubinemia with liver failure that resolved with glucocorticoid and mineralocorticoid treatment. Prompt recognition of this disease is imperative for timely intervention.

Impact of Clomiphene Citrate on the Steroid Profile in Dysmetabolic Men with Low Testosterone Levels

2021 ◽  
Vol 53 (08) ◽  
pp. 520-528
Author(s):  
Carla Pelusi ◽  
Flamina Fanelli ◽  
Margherita Baccini ◽  
Giovanni De Pergola ◽  
Vincenzo Triggiani ◽  
...  
Keyword(s):  
Clomiphene Citrate ◽  
Serum Levels ◽  
Male Hypogonadism ◽  
Hormonal Changes ◽  
Double Blind ◽  
Adrenal Steroidogenesis ◽  
Steroid Profiling ◽  
Corticosteroid Binding Globulin ◽  
Before And After ◽  
17Β Estradiol

AbstractClomiphene citrate (CC) in male hypogonadism increases testosterone (T) and estrogen levels by stimulating pituitary gonadotropin release. Our group confirmed these hormonal changes in a randomized, cross-over, double-blind trial of CC versus placebo in addition to metformin, conducted in 21 obese dysmetabolic men with low T levels. However, we hypothesize that based on its mechanism of action, CC may directly or indirectly affect adrenal steroidogenesis. The aim of this sub-study was to better understand the changes in steroid levels and metabolism induced by CC treatment. We assessed 17α-hydroxypregnelone (17αOH-P5), dehydroepiandrosterone (DHEA), progesterone (P4), 17α-hydroxyprogesterone (17αOH-P4), androstenedione (A), T, dihydrotestosterone (DHT), estrone (E1), 17β-estradiol (E2), 11-deoxycortisol (11 S), cortisol (F), and cortisone (E) by LC-MS/MS, and corticosteroid binding globulin (CBG) by ELISA, before and after each treatment. In addition, free-F and steroid product/precursor ratios were calculated. We observed a significant change in serum levels induced by CC compared with placebo for 17αOH-P4, DHT, T, E2, E1, F, E, and CBG, but not free-F. In addition, compared to placebo, CC induced higher 17αOH-P4/P4, E2/E1, 17αOH-P4/17αOH-P5, A/17αOH-P4, T/A, E1/A, F/11 S, and F/E ratios. Therefore, besides the CC stimulating effect on testis steroidogenesis, our study showed increased F, E, but not free-F, levels, indicating changes in steroid metabolism rather than adrenal secretion stimulation. The steroid profiling also revealed the CC stimulation of the Δ5 rather than the Δ4 pathway, thus indicating considerable testicular involvement in the increased androgen secretion.

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