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Relevant bibliographies by topics / 11B-HSD1

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Academic literature on the topic '11B-HSD1'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "11B-HSD1"

1

Du, Hanze, Limei Liu, Ying Wang, Yuichi Nakagawa, Alexei Lyzlov, Kabirullah Lutfy, Theodore C. Friedman, Xiaozhong Peng, and Yanjun Liu. "Specific reduction of G6PT may contribute to downregulation of hepatic 11β-HSD1 in diabetic mice." Journal of Molecular Endocrinology 50, no. 2 (December 24, 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 antisense oligonucleotides (G6PT ASO) in the pre-receptor metabolism of glucocorticoids as related to glucose homeostasis and insulin tolerance by examining the production of 11β-HSD1 and H6PDH in both male db/+ and db/db mouse liver tissue. We observed that G6PT ASO treatment of db/db mice markedly reduced hepatic G6PT mRNA and protein levels and substantially diminished the activation of hepatic 11β-HSD1 and H6PDH. Reduction of G6pt expression was correlated with the suppression of both hepatic gluconeogenic enzymes G6Pase and PEPCK and corresponded to the improvement of hyperglycemia and insulin resistance in db/db mice. Addition of G6PT ASO to mouse hepa1–6 cells led to a dose-dependent decrease in 11B-Hsd1 production. Knockdown of G6PT with RNA interference also impaired 11B-Hsd1 expression and showed comparable effects to H6pdh siRNA on silencing of H6pdh and 11B-Hsd1 expression in these intact cells. These findings suggest that G6PT plays an important role in the modulation of pre-receptor activation of glucocorticoids and provides new insights into the role of G6PT in the development of type 2 diabetes.

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2

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 (August 2, 2013): P5688. http://dx.doi.org/10.1093/eurheartj/eht310.p5688.

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3

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 (October 9, 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 (March 18, 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, Mitsuhiro Kometani, Seigo Konishi, Takashi Sawamura, Yoshimichi Takeda, Yoshiyu Takeda, and Takashi Yoneda. "ODP145 Epigenesis of 11beta-hydroxysteroid dehydrogenase 1 in the adipose tissue of aldosterone-producing adenoma." Journal of the Endocrine Society 6, Supplement_1 (November 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 was diagnosed according to the guideline of the Japanese Endocrine Society. The expression levels of HSD11B1 mRNA were quantified using a real time PCR. Isolated DNA was treated with bisulfite and amplified using primers specific for the humanHSD11B1promoter region. Results The glycohemoglobin level was significantly higher in patients with APA compared with those with NFA (p<0. 05). Blood pressure was significantly elevated in patients with APA compared with those with NFA (p<0. 01). TheHSD11B1 mRNA level and the enzyme activities were significantly increased in the adipose tissues of APA compared with NFA patients (p<0. 05). The methylation ratio was not significantly different between APA and NFA patients. Conclusion These results may suggest that adipose11beta-HSD1 contributes to metabolic abnormalities in APA. The pathophysiological significance of epigenetic control of 11beta-HSD1 gene in the adipose tissue should be further studied. Presentation: No date and time listed

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6

Ritchie, Craig W., Scott Webster, Jeffrey L. Cummings, Colin L. Masters, Vincent Ruffles, Jonathan Seckl, and Brian R. Walker. "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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7

Asano, H., K. Shearman, A. Darnel, B. S. Richardson, and 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, no. 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 degree of associated fetal acidaemia, but there were no corresponding increases in the tissue level of 11β-HSD2 activity. Hence, a time lag may exist between the mRNA and activity. Alternatively, the translation of 11β-HSD2 mRNA may be inhibited. In contrast, levels of 11β-HSD1 mRNA in the placenta and fetal liver were unchanged 72 h after sustained hypoxaemia. These results indicate that sustained fetal hypoxaemia with metabolic acidosis selectively up-regulates 11β-HSD2 mRNA expression in the near-term fetal sheep kidney. This may be a re-bound effect at 72 h following an initial down-regulation as observed in a previous study.

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8

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

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9

Morgan, Stuart, Iwona Bujalska, Laura Gathercole, Zaki Hassan-Smith, Phil Guest, Lianne Abrahams, Paul Stewart, Gareth Lavery, and Jeremy Tomlinson. "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 a model of GC excess we demonstrate that 11β-HSD1 mediates the adverse metabolic effects of GC excess on a global scale. I further investigated brown adipose tissue (BAT) with GC excess. I demonstrate that 11β-HSD1 regulates BAT activity and mitochondrial function, possibly suppressing BATs thermogenic potential. I extended my studies to examine the potential for white adipose tissue (WAT) to assume markers of thermogneic and mitochondrial function in the context of 11βHSD1 and GC excess. The data suggest 11β-HSD1 may suppress the potential of WAT to assume a ‘BAT-like’ profile. These data show 11β-HSD1 loss of function confers a protective phenotype with GC excess and demonstrates it’s role in mediating the metabolic phenotype associated with GCs. These data support the idea that GCs can influence BAT and WAT thermogenic potential and may increase knowledge of metabolic dysregulation in humans suffering form GC excess. This therefore highlights 11β-HSD1 as an exciting potential target for the treatment for the metabolic disease associated with GC excess.

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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 expression and activity are stimulated by a combined treatment of estradiol and medroxyprogesterone (used as analogue of progesterone). In parallel experiments, we demonstrated that also interleukin 1, alone and in combination with interferon-, has the ability to increase expression and activity of the enzyme. In the same work, that resulted in a paper published on Molecular and Cellular Endocrinology, we reported that elevated expression levels of 11B-HSD1 in decidua correlated with development of preeclampsia, suggesting a possible implication of the enzyme also in a pathological onset. In the second section, I investigated the role of 11B-HSD1 in the second part of gestation, using a dual-model approach involving murine and human uterus. We demonstrated the close correlation between pregnancy progression and 11B-HSD1 expression levels. In particular, after an early stable state, we observed a progressive increase of the mRNA and protein expression of the enzyme from mid-pregnancy to the last day of murine pregnancy, followed by an expression drop at the onset of labour. Our experiments with human cells reported also that 11B-HSD1 is involved in myometrium contraction, suggesting that enzyme has an essential role also in the mechanism of labour. In the last part of my thesis, I explored the skin pathology of psoriasis and one of its possible medical treatments, narrow-band UVB irradiation. In our preliminary experiments, we studied the expression levels of 11B-HSD1 before and after this medical approach on psoriatic patients, comparing results with control subjects. Our findings showed that controls and patients before the treatments have similar 11B-HSD1 expression levels. After the treatment period, mRNA and protein expression of the enzyme significantly rose up, suggesting a possible involvement of the 11-HSD1 in the molecular mechanism of the symptoms improvement. Globally, we reported a new vision of 11B-HSD1, with involvement in physiology and pathology of gestation and skin, never observed in previous reports, highlighting new perspectives in roles and ‘specific weight’ of the enzyme in organs and tissues different from the classic targets of 11B-HSD1.

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