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Glucocorticoid deficiency

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https://www.readbyqxmd.com/read/28089708/hair-corticosterone-measurement-in-mouse-models-of-type-1-and-type-2-diabetes-mellitus
#1
Rebecca L Erickson, Caroline A Browne, Irwin Lucki
In diabetes, glucocorticoid secretion increases secondary to hyperglycemia and is associated with an extensive list of disease complications. Levels of cortisol in humans, or corticosterone in rodents, are usually measured as transitory biomarkers of stress in blood or saliva. Glucocorticoid concentrations accumulate in human or animal hair over weeks and could more accurately measure the cumulative stress burden of diseases like chronic diabetes. In this study, corticosterone levels were measured in hair in verified rodent models of diabetes mellitus...
January 12, 2017: Physiology & Behavior
https://www.readbyqxmd.com/read/28069032/glucocorticoid-receptor-gene-polymorphisms-in-hereditary-angioedema-with-c1-inhibitor-deficiency
#2
Zsuzsanna Zotter, Zsolt Nagy, Attila Patócs, Dorottya Csuka, Nóra Veszeli, Kinga Viktória Kőhalmi, Henriette Farkas
BACKGROUND: Hereditary angioedema caused by C1-inhibitor deficiency (C1-INH-HAE) is a rare, autosomal dominant disorder. C1-INH-HAE is characterized by edema-formation, which may occur in response to stress. The individual's response to stress stimuli is partly genetically determined. Activation of the hypothalamic-pituitary-adrenal axis results in the release of cortisol. In turn, the secreted gluco- and mineralocorticoids affect the metabolism, as well as the cardiovascular and immune systems...
January 10, 2017: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/28065637/the-steroid-metabolite-16-%C3%AE-oh-androstenedione-generated-by-cyp21a2-serves-as-a-substrate-for-cyp19a1
#3
J Neunzig, M Milhim, L Schiffer, Y Khatri, J Zapp, A Sánchez-Guijo, M F Hartmann, S A Wudy, R Bernhardt
The 21-hydroxylase (CYP21A2) is a steroidogenic enzyme crucial for the synthesis of mineralo- and glucocorticoids. It is described to convert progesterone as well as 17-OH-progesterone, through a hydroxylation at position C21, into 11-deoxycorticosterone (DOC) and 11-deoxycortisol (RSS), respectively. In this study we unraveled CYP21A2 to have a broader steroid substrate spectrum than assumed. Utilizing a reconstituted in vitro system, consisting of purified human CYP21A2 and human cytochrome P450 reductase (CPR) we demonstrated that CYP21A2 is capable to metabolize DOC, RSS, androstenedione (A4) and testosterone (T)...
January 5, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28040534/cardiovascular-risk-factors-in-survivors-of-childhood-hematopoietic-cell-transplantation-treated-with-total-body-irradiation-a-longitudinal-analysis
#4
Danielle Novetsky Friedman, Patrick Hilden, Chaya S Moskowitz, Maya Suzuki, Farid Boulad, Nancy Kernan, Suzanne Wolden, Kevin C Oeffinger, Charles A Sklar
Hematopoietic cell transplantation (HCT) survivors treated with total body irradiation (TBI) are known to be at increased risk for the development of cardiovascular risk factors (CVRFs). We sought to characterize the incidence of CVRFs in a TBI-exposed survivor cohort and to describe prognostic indicators of their development through a retrospective analysis of CVRFs in 1-year survivors of leukemia or lymphoma treated with TBI at Memorial Sloan Kettering between April 1987 and May 2011. Eligible participants were age ≤21 years at the time of TBI and were not receiving glucocorticoid therapy at the time of entry to long-term follow-up...
December 28, 2016: Biology of Blood and Marrow Transplantation
https://www.readbyqxmd.com/read/28004974/vitamin-d3-protects-against-prednisolone-induced-liver-injury-associated-with-the-impairment-of-the-hepatic-nf-%C3%AE%C2%BAb-inos-no-pathway
#5
Olha Lisakovska, Ihor Shymanskyy, Anna Mazanova, Anna Khomenko, Mykola Veliky
The study was carried out to define whether prednisolone-induced damage to hepatic cells is accompanied by excessive nitric oxide (NO) levels associated with nuclear factor kappa B (NF-κB)/inducible NO synthase (iNOS) activation and evaluate the efficacy of the treatment with vitamin D3. Histopathological examination, activities of liver transaminases (alanine aminotransferase and aspartate aminotransferase), and cell death assays consistently showed that prednisolone (5 mg/kg body weight, 30 days) induces chronic liver injury in female Wistar rats...
July 14, 2016: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/27979924/tumor-suppressors-btg1-and-ikzf1-cooperate-during-mouse-leukemia-development-and-increase-relapse-risk-in-b-cell-precursor-acute-lymphoblastic-leukemia-patients
#6
Blanca Scheijen, Judith M Boer, Rene' Marke, Esther Tijchon, Dorette van Ingen Schenau, Esme' Waanders, Liesbeth van Emst, Laurens T van der Meer, Rob Pieters, Gabriele Escherich, Martin A Horstmann, Edwin Sonneveld, Nicola Venn, Rosemary Sutton, Luciano Dalla-Pozza, Roland P Kuiper, Peter M Hoogerbrugge, Monique L den Boer, Frank N van Leeuwen
Deletions and mutations affecting lymphoid transcription factor IKZF1 (IKAROS) are associated with an increased relapse risk and poor outcome in B-cell precursor acute lymphoblastic leukemia. However, additional genetic events may either enhance or negate the effects of IKZF1 deletions on prognosis. In a large discovery cohort of 533 childhood B-cell precursor acute lymphoblastic leukemia patients, we observed that single copy losses of BTG1 were significantly enriched in IKZF1-deleted B-cell precursor acute lymphoblastic leukemia (P=0...
December 15, 2016: Haematologica
https://www.readbyqxmd.com/read/27959413/17%C3%AE-%C3%A2-hydroxylase-17-20%C3%A2-lyase-deficiency-in-congenital-adrenal-hyperplasia-a-case-report
#7
Simiao Xu, Shuhong Hu, Xuefeng Yu, Muxun Zhang, Yan Yang
Congenital adrenal hyperplasia (CAH) is a rare autosomal recessive disorder caused by mutations in the cytochrome P450 family 17 subfamily A member 1 (CYP17A1) gene located on chromosome 10q24.3, which leads to a deficiency in 17α‑hydroxylase/17,20‑lyase. The disorder is characterized by low blood levels of estrogens, androgens and cortisol, which leads to a compensatory increase in adrenocorticotropic hormone levels that stimulate the production of mineralocorticoid precursors. This subsequently leads to hypertension, hypokalemia, primary amenorrhea and sexual infantilism...
January 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27941970/extensive-regulation-of-diurnal-transcription-and-metabolism-by-glucocorticoids
#8
Benjamin D Weger, Meltem Weger, Benjamin Görling, Andrea Schink, Cédric Gobet, Céline Keime, Gernot Poschet, Bernard Jost, Nils Krone, Rüdiger Hell, Frédéric Gachon, Burkhard Luy, Thomas Dickmeis
Altered daily patterns of hormone action are suspected to contribute to metabolic disease. It is poorly understood how the adrenal glucocorticoid hormones contribute to the coordination of daily global patterns of transcription and metabolism. Here, we examined diurnal metabolite and transcriptome patterns in a zebrafish glucocorticoid deficiency model by RNA-Seq, NMR spectroscopy and liquid chromatography-based methods. We observed dysregulation of metabolic pathways including glutaminolysis, the citrate and urea cycles and glyoxylate detoxification...
December 2016: PLoS Genetics
https://www.readbyqxmd.com/read/27940765/management-of-children-with-hereditary-angioedema-due-to-c1-inhibitor-deficiency
#9
Michael M Frank, Bruce Zuraw, Aleena Banerji, Jonathan A Bernstein, Timothy Craig, Paula Busse, Sandra Christiansen, Marc Davis-Lorton, H Henry Li, William R Lumry, Marc Riedl
Hereditary angioedema (HAE) is a potentially life-threatening inherited disease characterized by attacks of skin swelling, severe abdominal pain, and upper airway swelling. Attacks typically begin in childhood, but the appropriate diagnosis is often missed. Attacks do not respond to epinephrine, antihistamines, or glucocorticoids. Recently, many effective drugs have been approved for treatment of adults with HAE, and the Medical Advisory Board of the HAE Patient's Association has developed and reported treatment recommendations for adults...
November 2016: Pediatrics
https://www.readbyqxmd.com/read/27928728/clinical-perspectives-in-congenital-adrenal-hyperplasia-due-to-11%C3%AE-hydroxylase-deficiency
#10
REVIEW
Krupali Bulsari, Henrik Falhammar
Congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency is a rare autosomal recessive genetic disorder. It is caused by reduced or absent activity of 11β-hydroxylase (CYP11B1) enzyme and the resultant defects in adrenal steroidogenesis. The most common clinical features of 11 beta-hydroxylase deficiency are ambiguous genitalia, accelerated skeletal maturation and resultant short stature, peripheral precocious puberty and hyporeninemic hypokalemic hypertension. The biochemical diagnosis is based on raised serum 11-deoxycortisol and 11-deoxycorticosterone levels together with increased adrenal androgens...
December 7, 2016: Endocrine
https://www.readbyqxmd.com/read/27905124/assessment-of-early-atherosclerosis-and-left-ventricular-dysfunction-in-children-with-21-hydroxylase-deficiency
#11
Rahmi Özdemir, Hüseyin Anil Korkmaz, Mehmet Küçük, Cem Karadeniz, Timur Meşe, Behzat Özkan
AIM: We analysed 25 children with 21-hydroxylase deficiency who received glucocorticoid and/or mineralocorticoid treatment for at least 12 months to determine the effects of the disease and its treatment on vascular structures and ventricular function. METHODS: Twenty-five patients with 21-hydroxylase-deficient congenital adrenal hyperplasia (CAH) and 25 control subjects were enrolled into this observational, cross-sectional study. The patients were investigated in terms of fasting blood glucose and insulin; fasting serum lipid profile; serum 17-hydroxyprogesterone; dehydroepiandrosterone sulphate; androstenedione; and adrenocorticotropic hormone...
November 7, 2016: Clinical Endocrinology
https://www.readbyqxmd.com/read/27898652/natural-mineral-rich-water-ingestion-by-ovariectomized-fructose-fed-sprague-dawley-rats-effects-on-sirtuin-1-and-glucocorticoid-signaling-pathways
#12
Jugal Kishore Das, Milton Severo, Cidália Dionísio Pereira, Emília Patrício, José Magalhães, Rosário Monteiro, Delminda Neves, Maria João Martins
OBJECTIVE: Prevention or induction of metabolic disorders and obesity depend on estrogen signaling and/or exogenous factors, such as mineral content in diet. The protective effects of a Portuguese natural mineral-rich water against the induction of metabolic syndrome in fructose-fed male Sprague-Dawley rats have been reported. The present study was designed to assess the impact of this mineral-rich water on fructose-fed estrogen-deficient female Sprague-Dawley rats. METHODS: Ovariectomized rats had access to tap (TWO) or mineral-rich (MWO) waters, with and without 10% fructose (10-wk treatment)...
November 28, 2016: Menopause: the Journal of the North American Menopause Society
https://www.readbyqxmd.com/read/27885053/11%C3%AE-hydroxysteroid-dehydrogenase-1-deficiency-alters-the-gut-microbiome-response-to-western-diet
#13
Jethro S Johnson, Monica N Opiyo, Marian Thomson, Karim Gharbi, Jonathan R Seckl, Andreas Heger, Karen E Chapman
The enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD) interconverts active glucocorticoids and their intrinsically inert 11-keto forms. The type 1 isozyme, 11β-HSD1, predominantly reactivates glucocorticoids in vivo and can also metabolise bile acids. 11β-HSD1-deficient mice show altered inflammatory responses and are protected against the adverse metabolic effects of a high-fat diet. However, the impact of 11β-HSD1 on the composition of the gut microbiome has not previously been investigated. We used high-throughput 16S rDNA amplicon sequencing to characterise the gut microbiome of 11β-HSD1-deficient and C57Bl/6 control mice, fed either a standard chow diet or a cholesterol- and fat-enriched 'Western' diet...
February 2017: Journal of Endocrinology
https://www.readbyqxmd.com/read/27871077/impact-of-annexin-a-7-deficiency-on-fgf23-plasma-concentrations
#14
Anja T Umbach, Omar El-Attar, Dong Luo, Hajar Fakhri, Rosi Bissinger, Florian Lang
BACKGROUND/AIMS: The release of fibroblast growth factor FGF23, a powerful regulator of 1,25(OH)2D3 formation and mineral metabolism, is stimulated by store-operated Ca2+ entry (SOCE), which is accomplished by the pore forming Ca2+ release activated channel protein Orai1. Regulators of Orai1 and thus FGF23 release include serum & glucocorticoid inducible kinase SGK1, a kinase up-regulated by glucocorticosteroids. Some effects of glucocorticoids require the presence of annexin A7, such as suppression of prostaglandin E2 in gastric glands...
2016: Kidney & Blood Pressure Research
https://www.readbyqxmd.com/read/27870896/m30-antagonizes-indoleamine-2-3-dioxygenase-activation-and-neurodegeneration-induced-by-corticosterone-in-the-hippocampus
#15
Chun-Sing Lam, George Lim Tipoe, Johnny Kong-Ching Wong, Moussa B H Youdim, Man-Lung Fung
Monoamine oxidases (MAO), downstream targets of glucocorticoid, maintain the turnover and homeostasis of monoamine neurotransmitters; yet, its pathophysiological role in monoamine deficiency, oxidative stress and neuroinflammation remains controversial. Protective effects of M30, a brain selective MAO inhibitor with iron-chelating antioxidant properties, have been shown in models of neurodegenerative diseases. This study aims to examine the neuroprotective mechanism of M30 against depressive-like behavior induced by corticosterone (CORT)...
2016: PloS One
https://www.readbyqxmd.com/read/27861175/transient-receptor-potential-vanilloid-4-and-serum-glucocorticoid-regulated-kinase-1-are-critical-mediators-of-lung-injury-in-overventilated-mice-in-vivo
#16
Laura Michalick, Lasti Erfinanda, Ulrike Weichelt, Markus van der Giet, Wolfgang Liedtke, Wolfgang M Kuebler
BACKGROUND: Mechanical ventilation can cause lung endothelial barrier failure and inflammation cumulating in ventilator-induced lung injury. Yet, underlying mechanotransduction mechanisms remain unclear. Here, the authors tested the hypothesis that activation of the mechanosensitive Ca channel transient receptor potential vanilloid (TRPV4) by serum glucocorticoid-regulated kinase (SGK) 1 may drive the development of ventilator-induced lung injury. METHODS: Mice (total n = 54) were ventilated for 2 h with low (7 ml/kg) or high (20 ml/kg) tidal volumes and assessed for signs of ventilator-induced lung injury...
February 2017: Anesthesiology
https://www.readbyqxmd.com/read/27859809/forebrain-specific-transgene-rescue-of-11%C3%AE-hsd1-associates-with-impaired-spatial-memory-and-reduced-hippocampal-bdnf-mrna-levels-in-aged-11%C3%AE-hsd1-deficient-mice
#17
Sarah Caughey, Anjanette P Harris, Jonathan R Seckl, Megan C Holmes, Joyce L W Yau
Mice lacking the intracellular glucocorticoid-regenerating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) are protected from age-related spatial memory deficits. 11β-HSD1 is expressed predominantly in brain, liver and adipose tissue. Reduced glucocorticoid levels in brain in the absence of 11β-HSD1 may underlie the improved memory in aged 11β-HSD1 deficient mice. However, the improved glucose tolerance, insulin sensitization and cardio-protective lipid profile associated with reduced peripheral glucocorticoid regeneration may potentially contribute to the cognitive phenotype of aged 11β-HSD1 deficient mice...
November 17, 2016: Journal of Neuroendocrinology
https://www.readbyqxmd.com/read/27856527/role-of-glucocorticoid-receptor-and-pregnane-x-receptor-in-dexamethasone-induction-of-rat-hepatic-aryl-hydrocarbon-receptor-nuclear-translocator-and-nadph-cytochrome-p450-oxidoreductase
#18
Sarah R Hunter, Alex Vonk, Anne K Mullen Grey, David S Riddick
The aryl hydrocarbon receptor (AHR) nuclear translocator (ARNT), as the AHR's heterodimerization partner, and NADPH-cytochrome P450 oxidoreductase (POR), as the key electron donor for all microsomal P450s, are independent and indispensable components in the adaptive and toxic responses to polycyclic aromatic hydrocarbons. Expression of both ARNT and POR in rat liver is induced by dexamethasone (DEX), a synthetic glucocorticoid known to activate both the glucocorticoid receptor (GR) and the pregnane X receptor (PXR)...
November 16, 2016: Drug Metabolism and Disposition: the Biological Fate of Chemicals
https://www.readbyqxmd.com/read/27834956/a-bak-dependent-mitochondrial-amplification-step-contributes-to-smac-mimetic-glucocorticoid-induced-necroptosis
#19
Katharina Rohde, Lara Kleinesudeik, Stefanie Roesler, Oliver Löwe, Juliana Heidler, Katrin Schröder, Ilka Wittig, Stefan Dröse, Simone Fulda
Necroptosis is a form of programmed cell death that critically depends on RIP3 and MLKL. However, the contribution of mitochondria to necroptosis is still poorly understood. In the present study, we discovered that mitochondrial perturbations play a critical role in Smac mimetic/Dexamethasone (Dexa)-induced necroptosis independently of death receptor ligands. We demonstrate that the Smac mimetic BV6 and Dexa cooperate to trigger necroptotic cell death in acute lymphoblastic leukemia (ALL) cells that are deficient in caspase activation due to absent caspase-8 expression or pharmacological inhibition by the caspase inhibitor zVAD...
January 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27829137/tumor-induced-il-6-reprograms-host-metabolism-to-suppress-anti-tumor-immunity
#20
Thomas R Flint, Tobias Janowitz, Claire M Connell, Edward W Roberts, Alice E Denton, Anthony P Coll, Duncan I Jodrell, Douglas T Fearon
In patients with cancer, the wasting syndrome, cachexia, is associated with caloric deficiency. Here, we describe tumor-induced alterations of the host metabolic response to caloric deficiency that cause intratumoral immune suppression. In pre-cachectic mice with transplanted colorectal cancer or autochthonous pancreatic ductal adenocarcinoma (PDA), we find that IL-6 reduces the hepatic ketogenic potential through suppression of PPARalpha, the transcriptional master regulator of ketogenesis. When these mice are challenged with caloric deficiency, the resulting relative hypoketonemia triggers a marked rise in glucocorticoid levels...
November 8, 2016: Cell Metabolism
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