Nutritional marginal zinc deficiency disrupts placental 11β-hydroxysteroid dehydrogenase type 2 modulation

2016 ◽  
Vol 7 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Y. L. Huang ◽  
S. Supasai ◽  
H. Kucera ◽  
N. W. Gaikwad ◽  
A. M. Adamo ◽  
...  
Keyword(s):  
Zinc Deficiency ◽  
Hydroxysteroid Dehydrogenase ◽  
Fetal Exposure ◽  
Marginal Zinc Deficiency ◽  
Zinc Nutrition

This paper investigated if marginal zinc nutrition during gestation could affect fetal exposure to glucocorticoids as a consequence of a deregulation of placental 11βHSD2 expression.

Proinflammatory cytokines inhibit human placental 11β-hydroxysteroid dehydrogenase type 2 activity through Ca2+ and cAMP pathways

2006 ◽  
Vol 290 (2) ◽  
pp. E282-E288 ◽  
Author(s):  
Iren Kossintseva ◽  
Susan Wong ◽  
Ed Johnstone ◽  
Larry Guilbert ◽  
David M. Olson ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Adenylyl Cyclase ◽  
Proinflammatory Cytokines ◽  
Hydroxysteroid Dehydrogenase ◽  
Mrna Levels ◽  
Fetal Exposure ◽  
Increased Risk ◽  
Tnf Α ◽  
Intracellular Ca

Excessive fetal exposure to glucocorticoids has been implicated in the etiology of adult metabolic and cardiovascular disease. Placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) may protect the fetus from excessive glucocorticoid exposure. Maternal stress may be accompanied by elevated levels of cortisol and increased proinflammatory cytokines [interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)]. We hypothesize that proinflammatory cytokines inhibit human placental 11β-HSD activity. We incubated explant cultures of term human placental villi in the presence or absence of 10 ng/ml IL-1β, IL-6, or TNF-α, with or without agonists or antagonists of intracellular Ca2+ and adenylyl cyclase. Activity for 11β-HSD2 was estimated using a radioisotope assay, and mRNA was measured using quantitative RT-PCR. All cytokines significantly ( P ≤ 0.05) reduced 11β-HSD2 activity (>75% suppression); maximal inhibition occurred within 2 h and was maintained for at least 24 h. The IL-1β-induced inhibitory activity was attenuated using a Ca2+ channel blocker (nifedipine), an intracellular Ca2+ antagonist [8-( N, N-diethylamino)octyl-3,4,5-trimethoxybenzoate], or the adenylyl cyclase stimulant forskolin. Conversely, 11β-HSD2 activity was diminished in the presence of the Ca2+ ionophore A-23187 or the adenylyl cyclase inhibitor SQ-22536. mRNA levels for 11β-HSD2 were not changed by any of the treatments. Proinflammatory cytokines inhibit human placental 11β-HSD2 activity through a mechanism that involves increased intracellular Ca2+ and inhibition of adenylyl cyclase. This could result in excessive fetal exposure to maternal cortisol. This mechanism might mediate part of the increased risk of metabolic and cardiovascular disease in adult offspring.

scholarly journals Cloning and production of antisera to human placental 11 β-hydroxysteroid dehydrogenase type 2

1996 ◽  
Vol 313 (3) ◽  
pp. 1007-1017 ◽  
Author(s):  
Roger W. BROWN ◽  
Karen E. CHAPMAN ◽  
Yuri KOTELEVTSEV ◽  
Joyce L. W. YAU ◽  
Robbie S. LINDSAY ◽  
...  
Keyword(s):  
Reductase Activity ◽  
Hydroxysteroid Dehydrogenase ◽  
Fetal Exposure ◽  
Adult Kidney ◽  
Peptide Carrier ◽  
Affinity Labelling ◽  
Ic50 Values ◽  
20 Nm

By inactivating potent glucocorticoid hormones (cortisol and corticosterone), 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) plays an important role in the placenta by controlling fetal exposure to maternal glucocorticoids, and in aldosterone target tissues by controlling ligand access to co-localized glucocorticoid and mineralocorticoid receptors. Amino acid sequence from homogeneous human placental 11β-HSD2 was used to isolate a 1897 bp cDNA encoding this enzyme (predicted Mr 44126; predicted pI 9.9). Transfection into mammalian (CHO) cells produces 11β-HSD2 activity which is NAD+-dependent, is without reductase activity, avidly metabolizes glucocorticoids (Km values for corticosterone, cortisol and dexamethasone of 12.4±1.5, 43.9±8.5 and 119±15 nM respectively) and is inhibited by glycyrrhetinic acid and carbenoxolone (IC50 values 10–20 nM). Rabbit antisera recognizing 11β-HSD2 have been raised to an 11β-HSD2-(370–383)-peptide–carrier conjugate. Recombinant 11β-HSD2, like native human placental 11β-HSD2, is detectable with affinity labelling and anti-11β-HSD2 antisera, and appears to require little post-translational processing for activity. 11β-HSD2 mRNA (~1.9 kb transcript) is expressed in placenta, aldosterone target tissues (kidney, parotid, colon and skin) and pancreas. In situ hybridization and immunohistochemistry localize abundant 11β-HSD2 expression to the distal nephron in human adult kidney and to the trophoblast in the placenta. 11β-HSD2 transcripts are expressed in fetal kidney (but not lung, liver or brain) at 21–26 weeks, suggesting that an 11β-HSD2 distribution resembling that in the adult is established by this stage in human development.

scholarly journals Evaluation of Serum Zinc Status of Pregnant Women in the China Adult Chronic Disease and Nutrition Surveillance (CACDNS) 2015

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1375
Author(s):  
Xiao-Bing Liu ◽  
Jia-Xi Lu ◽  
Li-Juan Wang ◽  
Yi-Chun Hu ◽  
Rui Wang ◽  
...  
Keyword(s):  
Chronic Disease ◽  
Pregnant Women ◽  
Zinc Deficiency ◽  
Evaluation System ◽  
Family Income ◽  
Serum Zinc ◽  
Zinc Status ◽  
National Monitoring ◽  
Significant Difference ◽  
Zinc Nutrition

Objective: The purpose of this study was to evaluate serum zinc status of pregnant women in the China Adult Chronic Disease and Nutrition Surveillance (CACDNS) in 2015–2016. Methods: A total of 7147 apparently healthy pregnant women were randomly selected in 302 national monitoring sites. Information on age, race, residence region, education, pregnancy, and family income per annum was collected, and the concentration of serum zinc was determined. The evaluation of serum zinc status was further performed according to the recommendations by the International Zinc Nutrition Consultative Group (IZiNCG). Results: The median concentration of serum zinc was 858.9 μg/L with an interquartile range (IQR) of 712.9 μg/L and 1048.9 μg/L, while the overall prevalence of zinc deficiency was 3.5% with a 95% confidence interval (CI) of 3.0% and 3.9%. Serum zinc status of pregnant women changed greatly in the different categories, particular in pregnancy and family income per annum (p < 0.05), but no significant difference was observed in the prevalence of zinc deficiency (p > 0.05). Conclusions: The lower prevalence of zinc deficiency generally indicated a better zinc status for pregnant women in the CACDNS in 2015–2016. However, a well-designed evaluation system of zinc status for pregnant women should be continually optimized and improved by inducing more parameters such as biochemical, dietary, or functional indicators.

scholarly journals Synthesis, purification and crystallographic studies of the C-terminal sterol carrier protein type 2 (SCP-2) domain of human hydroxysteroid dehydrogenase-like protein 2

2015 ◽  
Vol 71 (7) ◽  
pp. 901-905 ◽  
Author(s):  
Zhong Cheng ◽  
Yao Li ◽  
Chun Sui ◽  
Xiaobo Sun ◽  
Yong Xie
Keyword(s):  
Catalytic Domain ◽  
Hydroxysteroid Dehydrogenase ◽  
Carrier Protein ◽  
Sterol Carrier Protein ◽  
X Ray Diffraction ◽  
Unit Cell Parameters ◽  
X Ray ◽  
Cell Parameters ◽  
Protein Molecules

Human hydroxysteroid dehydrogenase-like protein 2 (HSDL2) is a member of the short-chain dehydrogenase/reductase (SDR) subfamily of oxidoreductases and contains an N-terminal catalytic domain and a C-termianl sterol carrier protein type 2 (SCP-2) domain. In this study, the C-terminal SCP-2 domain of human HSDL2, including residues Lys318–Arg416, was produced inEscherichia coli, purified and crystallized. X-ray diffraction data were collected to 2.10 Å resolution. The crystal belonged to the trigonal space groupP3121 (orP3221), with unit-cell parametersa=b= 70.4,c= 60.6 Å, α = β = 90, γ = 120°. Two protein molecules are present in the asymmetric unit, resulting in a Matthews coefficient of 2.16 Å3 Da−1and an approximate solvent content of 43%.

scholarly journals Marginal Zinc Deficiency and Changes in Behavioral Salt Taste Threshold and Salt Preference in Mice.

1991 ◽  
Vol 37 (2) ◽  
pp. 185-199 ◽  
Author(s):  
Xing-Wang LIU ◽  
Yasushi DEJIMA ◽  
Tsuguyoshi SUZUKI ◽  
Sei-ichiro HIMENO ◽  
Yoichi OKAZAKI
Keyword(s):  
Zinc Deficiency ◽  
Taste Threshold ◽  
Salt Taste ◽  
Marginal Zinc Deficiency

11β Hydroxysteroid Dehydrogenase Type 2 in the Adrenal Gland by Testosterone Withdrawal of Adult Rats

Folia Medica ◽  
2010 ◽  
Vol 52 (2) ◽  
Author(s):  
Yvetta Koeva ◽  
Mariana Bakalska ◽  
Elisaveta Petrova ◽  
Nina Atanassova
Keyword(s):  
Adrenal Gland ◽  
Hydroxysteroid Dehydrogenase ◽  
Adult Rats

11β hydroxysteroid dehydrogenase type 2 enzyme is expressed in normotensive and hypertensive patients with renal disease

Nephrology ◽  
2008 ◽  
Vol 4 (1-2) ◽  
pp. 81-86
Author(s):  
Alicia N STEIN-OAKLEY ◽  
Julie A MAGUIRE ◽  
John DOWLING ◽  
Greg J PERRY ◽  
Zygmunt KROZOWSKI ◽  
...  
Keyword(s):  
Renal Disease ◽  
Hydroxysteroid Dehydrogenase ◽  
Hypertensive Patients

Effects of maternal marginal zinc deficiency on myelin protein profiles in the suckling rat and infant rhesus monkey

1992 ◽  
Vol 34 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Hueyjiuan Liu ◽  
Patricia I. Oteiza ◽  
M. Eric Gershwin ◽  
Mari S. Golub ◽  
Carl L. Keen
Keyword(s):  
Rhesus Monkey ◽  
Zinc Deficiency ◽  
Myelin Protein ◽  
Protein Profiles ◽  
Marginal Zinc Deficiency ◽  
Infant Rhesus

scholarly journals 11?-Hydroxysteroid dehydrogenase Type 1 in obesity and Type 2 diabetes

Diabetologia ◽  
2004 ◽  
Vol 47 (1) ◽  
pp. 1-11 ◽  
Author(s):  
T. M. Stulnig ◽  
W. Waldh�usl
Keyword(s):  
Type 2 Diabetes ◽  
Hydroxysteroid Dehydrogenase
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