scholarly journals Ovarian modulators of 11beta-hydroxysteroid dehydrogenase (11betaHSD) activity in follicular fluid from gonadotrophin-stimulated assisted conception cycles

Reproduction ◽  
2002 ◽  
pp. 801-812 ◽  
Author(s):  
LM Thurston ◽  
DP Norgate ◽  
KC Jonas ◽  
C Chandras ◽  
HJ Kloosterboer ◽  
...  
Keyword(s):  
Follicular Fluid ◽  
Rat Kidney ◽  
Hydroxysteroid Dehydrogenase ◽  
Controlled Ovarian Hyperstimulation ◽  
Ovarian Hyperstimulation ◽  
Assisted Conception ◽  
Human Follicular Fluid ◽  
Glucocorticoid Metabolism ◽  
Stimulation Of

In the ovary, cortisol-cortisone interconversion is catalysed by isoforms of 11beta-hydroxysteroid dehydrogenase (11betaHSD). The objective of this study was to establish whether human follicular fluid (hFF), obtained after controlled ovarian hyperstimulation, contains paracrine modulators of 11betaHSD activity. Of 274 hFF samples tested for effects in rat kidney homogenates, 206 hFF samples significantly inhibited NADP(+)-dependent oxidation of cortisol within 1 h (by 11-67% of control 11betaHSD activity), whereas 42 hFF samples significantly stimulated 11betaHSD activity (16-210% increase relative to control). Although charcoal-stripping of hFF prevented the inhibition and potentiated the stimulation of NADP(+)-dependent cortisol oxidation in a renal homogenate, effects of individual hFF samples on NADP(+)-dependent cortisol oxidation were independent of intrafollicular progesterone concentrations. Hydrophilic fractions of hFF samples, isolated by C18 column chromatography, stimulated both the NADP(+)-dependent oxidation of cortisol (by 55+/-5%, n=98) and the NADPH-dependent reduction of cortisone (by 86+/-22%, n= 5). In contrast, the hydrophobic fractions of hFF (eluted at 65-85% methanol) inhibited both NADP(+)-dependent 11beta-dehydrogenase and NADPH-dependent 11-ketosteroid reductase activities (by 63+/-2% and 74+/-4%, respectively). None of the C18 column fractions of 50 hFF samples had any significant effect on NAD(+)-dependent 11beta-dehydrogenase activities. The hydrophobic inhibitors of NADP(H)-dependent cortisol-cortisone metabolism did not co-elute with several candidate compounds (prostaglandins E(2) and F(2alpha), cortisol, cortisone, oestradiol, testosterone, progesterone, pregnenolone or cholesterol). Hence, hFF aspirated from women undergoing controlled ovarian hyperstimulation for assisted conception contains both hydrophilic stimuli and hydrophobic inhibitors of glucocorticoid metabolism which appear to be selective for the NADP(H)-dependent, type 1 isoform of 11betaHSD.

scholarly journals Getting to the heart of intracellular glucocorticoid regeneration: 11β-HSD1 in the myocardium

2017 ◽  
Vol 58 (1) ◽  
pp. R1-R13 ◽  
Author(s):  
Gillian A Gray ◽  
Christopher I White ◽  
Raphael F P Castellan ◽  
Sara J McSweeney ◽  
Karen E Chapman
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Systemic Corticosteroid ◽  
Physiological Function ◽  
Pressure Overload ◽  
Hydroxysteroid Dehydrogenase ◽  
And Function ◽  
Glucocorticoid Metabolism

Corticosteroids influence the development and function of the heart and its response to injury and pressure overload via actions on glucocorticoid (GR) and mineralocorticoid (MR) receptors. Systemic corticosteroid concentration depends largely on the activity of the hypothalamic–pituitary–adrenal (HPA) axis, but glucocorticoid can also be regenerated from intrinsically inert metabolites by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), selectively increasing glucocorticoid levels within cells and tissues. Extensive studies have revealed the roles for glucocorticoid regeneration by 11β-HSD1 in liver, adipose, brain and other tissues, but until recently, there has been little focus on the heart. This article reviews the evidence for glucocorticoid metabolism by 11β-HSD1 in the heart and for a role of 11β-HSD1 activity in determining the myocardial growth and physiological function. We also consider the potential of 11β-HSD1 as a therapeutic target to enhance repair after myocardial infarction and to prevent the development of cardiac remodelling and heart failure.

scholarly journals Controlled ovarian hyperstimulation induced changes in the expression of circulatory miRNA in bovine follicular fluid and blood plasma

2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Sina Seifi Noferesti ◽  
Md. Mahmodul Hasan Sohel ◽  
Michael Hoelker ◽  
Dessie Salilew-Wondim ◽  
Ernst Tholen ◽  
...  
Keyword(s):  
Blood Plasma ◽  
Follicular Fluid ◽  
Controlled Ovarian Hyperstimulation ◽  
Ovarian Hyperstimulation ◽  
Induced Changes

scholarly journals 11β-hydroxysteroid dehydrogenase type 1 expression in 2S FAZA hepatoma cells is hormonally regulated: a model system for the study of hepatic glucocorticoid metabolism

1996 ◽  
Vol 317 (2) ◽  
pp. 621-625 ◽  
Author(s):  
Michael W. VOICE ◽  
Jonathan R. SECKL ◽  
Christopher R. W. EDWARDS ◽  
Karen E. CHAPMAN
Keyword(s):  
Mrna Expression ◽  
Hydroxysteroid Dehydrogenase ◽  
Proximal Promoter ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Transcription Start ◽  
Key Enzyme ◽  
Glucocorticoid Metabolism ◽  
Hepatic Cell Lines

11β-Hydroxysteroid dehydrogenase (11β-HSD) is a key enzyme in glucocorticoid metabolism, catalysing the conversion of active glucocorticoids into their inactive 11-keto metabolites, thus regulating glucocorticoid access to intracellular receptors. The type 1 isoform (11β-HSD 1) (EC 1.1.1.146) is widely distributed, with particularly high levels in liver, where accumulating evidence suggests that it acts as an 11β-reductase, regenerating active glucocorticoids. Investigation of the function and regulation of 11β-HSD 1 in liver has been hampered by the lack of hepatic cell lines which express 11β-HSD 1. Here, we describe 11β-HSD 1 mRNA expression and activity in 2S FAZA cells, a continuously cultured rat liver cell line. In intact 2S FAZA cells 11β-HSD 1 acts predominantly as a reductase, with very low dehydrogenase activity. In 2S FAZA cells 11β-HSD 1 activity and mRNA expression are regulated by hormones, with dexamethasone increasing activity and insulin, forskolin and insulin-like growth factor 1 decreasing it. Transfection of 2S FAZA cells with a luciferase reporter gene driven by the proximal promoter of the rat 11β-HSD 1 gene demonstrates that sequences which can mediate the responses to insulin, dexamethasone and forskolin all lie within 1800 bp of the transcription start site.

Follicular fluid lipid peroxidation levels in women with endometriosis during controlled ovarian hyperstimulation

2016 ◽  
Vol 20 (1) ◽  
pp. 48-54 ◽  
Author(s):  
Camila Bruna de Lima ◽  
Fernanda Bertuccez Cordeiro ◽  
Mariana Camargo ◽  
Daniel Suslik Zylbersztejn ◽  
Agnaldo Pereira Cedenho ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Follicular Fluid ◽  
Controlled Ovarian Hyperstimulation ◽  
Ovarian Hyperstimulation
Sign in / Sign up

Export Citation Format

Share Document