Relevant bibliographies by topics / 11B-HSD1

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Academic literature on the topic '11B-HSD1'

Author: Grafiati
Published: 14 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "11B-HSD1"

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Du, Hanze, Limei Liu, Ying Wang та ін. "Specific reduction of G6PT may contribute to downregulation of hepatic 11β-HSD1 in diabetic mice". Journal of Molecular Endocrinology 50, № 2 (2012): 167–78. http://dx.doi.org/10.1530/jme-12-0223.

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Pre-receptor activation of glucocorticoids via 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1 (HSD11B1)) has been identified as an important mediator of the metabolic syndrome. Hexose-6-phosphate dehydrogenase (H6PDH) mediates 11β-HSD1 amplifying tissue glucocorticoid production by driving intracellular NADPH exposure to 11β-HSD1 and requires glucose-6-phosphate transporter (G6PT (SLC37A4)) to maintain its activity. However, the potential effects of G6PT on tissue glucocorticoid production in type 2 diabetes and obesity have not yet been defined. Here, we evaluated the possible role of G6PT
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White, C., K. Mcgregor, K. Chapman, and G. Gray. "Does cardiovascular specific 11b-HSD1 deletion reproduce the beneficial effects of global 11b-HSD1 deficiency in the healing myocardial infarct?" European Heart Journal 34, suppl 1 (2013): P5688. http://dx.doi.org/10.1093/eurheartj/eht310.p5688.

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Guo, Jie, Li-Yan Zhou, Hong-Ping He, Ying Leng, Zhen Yang, and Xiao-Jiang Hao. "Inhibition of 11b-HSD1 by Tetracyclic Triterpenoids from Euphorbia kansui." Molecules 17, no. 10 (2012): 11826–38. http://dx.doi.org/10.3390/molecules171011826.

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Tyurenkov, Ivan Nikolaevich, Denis Vladimirovich Kurkin, Elena Vladimirovna Volotova, Dmitriy Alexandrovich Bakulin, and Elena Michailovna Lomkina. "Drug discovery for type 2 diabetes mellitus and metabolic syndrome: ten novel biological targets." Diabetes mellitus 18, no. 1 (2015): 101–9. http://dx.doi.org/10.14341/dm20151101-109.

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In this review we discuss ten promising biological targets of interest for treating type 2 diabetes mellitus, obesity and metabolic syndrome. Namely, we address current experimental and clinical data on several new compounds that affect SGLT2, 11b-HSD1, PTP1B, SCD1, Il-1?. , fructose-1,6-bisphosphatase, glycogen phosphorylase, SIRT1, DGAT-1 and GPR119. The body of data shows potential of these substances to become effective antidiabetic agents.
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Aono, Daisuke, Masashi Demura, Shigehiro Karashima, et al. "ODP145 Epigenesis of 11beta-hydroxysteroid dehydrogenase 1 in the adipose tissue of aldosterone-producing adenoma." Journal of the Endocrine Society 6, Supplement_1 (2022): A241. http://dx.doi.org/10.1210/jendso/bvac150.495.

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Abstract Objective 11Beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) is the key enzyme of metabolic syndrome. The transcript-specific epigenetic regulation of 11b-HSD1 (HSD11B1) is reported. We examined the HSD11B1 mRNA level and methylation status of the promoter region of the HSD11B1 in the adipose tissue of patients with aldosterone-producing adenoma (APA). Methods We evaluated 10 adipose tissue specimens from patients with primary aldosteronism due to aldosterone-producing adenoma (APA) and 7 tissue specimens from patients with non-functioning adrenal adenoma (NFA). Primary aldosteronism
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Ritchie, Craig W., Scott Webster, Jeffrey L. Cummings, et al. "P4-388: XANAMEMTM : A Novel 11B-HSD1 Inhibitor with Potential to Provide Durable Symptomatic and Disease Modifying Benefits in Alzheimer’S Disease." Alzheimer's & Dementia 12 (July 2016): P1186. http://dx.doi.org/10.1016/j.jalz.2016.07.133.

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Asano, H., K. Shearman, A. Darnel, B. S. Richardson та K. Yang. "Effects of sustained hypoxaemia with 72 hours recovery on 11β-hydroxysteroid dehydrogenase types 1 and 2 gene expression in near-term fetal sheep". Reproduction, Fertility and Development 9, № 8 (1997): 755. http://dx.doi.org/10.1071/r97070.

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The study examined the effects of 8 h sustained hypoxaemia, with 72 h recovery, on the expression of 11β-hydroxysteroid dehydrogenase (11b-HSD) types 1 and 2 in near-term fetal sheep. Placental tissue and fetal liver and kidney were collected at Days 135–138 gestation 72 h after 8 h sustained hypoxaemia induced by lowering maternal inspired oxygen with (n= 9) and without (n = 6) metabolic acidosis or after 8 h normoxia (n = 6). In hypoxic fetuses with metabolic acidosis, a significant increase in the level of 11β-HSD2 mRNA in the kidney compared with controls was correlated significantly with
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8

"11 β-hydroxysteroid dehydrogenase type 1 (HSD11B1; 11b HSD1)". Science-Business eXchange 1, № 25 (2008): 601. http://dx.doi.org/10.1038/scibx.2008.601.

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9

Heaselgrave, Samuel, Silke Heising, Stuart Andrew Morgan, et al. "SAT276 Glucocorticoid Excess Elevates Metabolic Rate Via A 11b-HSD1 Dependent Mechanism In C57BL/6J Mice." Journal of the Endocrine Society 7, Supplement_1 (2023). http://dx.doi.org/10.1210/jendso/bvad114.281.

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Abstract Disclosure: S. Heaselgrave: None. S. Heising: None. S.A. Morgan: None. A. Kabli: None. M. Sagmeister: None. C. Doig: None. R.S. Hardy: None. N.M. Morton: None. K. Tsintzas: None. G.G. Lavery: None. Introduction: Glucocorticoids are vital metabolic regulators. However, glucocorticoid excess (GE) causes severe metabolic dysfunction, ultimately leading to Cushing’s Syndrome. This dysfunction is often dependent on the presence of the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Whether GE also alters metabolic rate, and whether this is also dependent on 11β-HSD1, remains unc
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10

Morgan, Stuart, Iwona Bujalska, Laura Gathercole, et al. "11b-HSD1 knockout mice are protected from the adverse metabolic effects of exogenous glucocorticoid excess." Endocrine Abstracts, March 1, 2013, 1. http://dx.doi.org/10.1530/endoabs.31.oc4.2.

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Dissertations / Theses on the topic "11B-HSD1"

1

McCabe, Emma Louise. "Altering adipose tissue responses to glucocorticoids through genetic manipulation of the 11B-HSD1 gene." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6917/.

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Glucocorticoids (GC) are regulators of permissive and adaptive physiology. GC excess can lead to metabolic complications including type 2 diabetes and metabolic syndrome. Levels are regulated by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which reactivates GC. 11β-HSD1 activity is deregulated in a range metabolic disorders in which GC levels are normal. I hypothesise that 11β-HSD1 is a critical regulator of adipose tissue sensitivity to GC excess, and that through 11β-HSD1 depletion adipose tissue will be desensitised to GCs and resist metabolic deregulation. Using 11β-HSD1 KO mice in
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2

DAMIANI, FRANCESCO. "11ß-HSD1: novel roles and implications in pathology and physiology of reproduction and in skin homeostasis." Doctoral thesis, Università di Siena, 2017. http://hdl.handle.net/11365/1005619.

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My three-years work focused on the enzyme 11B-HSD1 and its implications and roles in human reproduction and skin homeostasis. The enzyme is involved in the local regulation of glucocorticoids availability, being responsible of the cortisone activation to cortisol. My project was composed of three major parts. In the first section, I analyzed the role of the enzyme in the human first trimester decidua. My experiments included a global evaluation of the enzyme susceptibility to respond to hormonal and cytokine stimuli, driving the first part of pregnancy. Our findings reported that 11B-HSD1 e
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