11β-Hydroxysteroid dehydrogenase type 1 is an important regulator at the interface of obesity and inflammation

Staab, Claudia A.; Maser, Edmund

doi:10.1016/j.jsbmb.2009.12.013

Cited by 96 publications

(83 citation statements)

References 239 publications

(293 reference statements)

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“…To ensure that differentiation was properly complied with, oil-red O staining was performed as previously reported by Nicholson et al 22 Cell treatment Differentiated cells in 6 well-plates (procedure described previously) were incubated in a restricted medium for 2 h (DMEM and Penicillin/Streptomycin). After restriction, the cells were treated with three different concentrations (0.1, 1, and 10 mM) of cortisone (Sigma-Aldrich, C2755) during 5 different time periods (5,10,15, and 20 min, and 48 h). The treatment medium was collected and utilized to identify time-dependent changes through quantification of glucose and free glycerol using the glucose oxidase-peroxidase method and the free glycerol determination kit (Sigma-Aldrich, FG0100-1KT), respectively.…”

Section: T3-l1 Cell Culturementioning

confidence: 99%

“…8 This led to the knowledge that the physiological action of GC on AT depends, in part, on their circulating levels and also, and importantly, on their tissue activation prior to impacting on their receptor, which occurs through 11b-Hydroxysteroid dehydrogenase 1 (Hsd1), the latter converting inactive cortisone into active cortisol. [9][10][11] The Matsuzaki et al 12 experiment solved this puzzle: it is the overexpression of Hsd1 that results in obesity and the Metabolic Syndrome (MS). In turn, knockout (KO) of Hsd1 protects against the obesity and hyperglycemia induced with a high-fat diet.…”

Section: Introductionmentioning

confidence: 99%

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HSD1 and AQP7 short-term gene regulation by cortisone in 3T3-L1 adipocytes

et al. 2016

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Adipose Tissue (AT) is a complex organ with a crucial regulatory role in energy metabolism and in the development of obesity and the Metabolic Syndrome (MS). Modified responses and the metabolism of hormones have been observed in visceral adiposity during obesity, specifically as related with cortisone. The objective of this study was to assess, in the 3T3-L1 adipocyte cell line, the short-term effect of cortisone on the expression of 11b-Hydroxysteroid dehydrogenase 1 (Hsd1), which is responsible for activation of cortisone into cortisol, and for Aquaporin 7 (Aqp7), involved in glycerol transport through the cell membrane. Total RNA (tRNA) and complementary DNA (cDNA) were obtained from cell samples treated with cortisone (0.1, 1, and 10 mM) during different times (0, 5, 10, 15, and 20 min, and 48 h) to quantify the expression of the aforementioned genes by real time PCR employing MnSOD and Ppia as housekeeping genes. There was a time-dependent response of Aqp7, a dose-dependent response of Hsd1, and an increase observed in the expression of both genes during min 1 of treatment (5-and 6-fold, respectively), followed by a decrease during the following 5-10 min (P < 0.05). With the 1-mM cortisone treatment, both genes showed cubic tendencies in their expression; the Hsd1 tendency is described by the equation y D 0.18£ 3 ¡1.65£ 2 C3.59xC1.31, while the Aqp7 tendency is described by y D 0.33£ 3 -2.67£ 2 C4.93xC1.84. There are immediate and quantitatively important actions of cortisone on the expression of Aqp7 and Hsd1 in 3T3-L1 adipocytes.

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Section: T3-l1 Cell Culturementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

HSD1 and AQP7 short-term gene regulation by cortisone in 3T3-L1 adipocytes

et al. 2016

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“…This complex set of hormone interactions is referred to as hypothalamic-pituitaryadrenal (HPA) axis. Cortisol regulates energy metabolism through gluconeogenesis, but also affects processes such as infl ammation (19,20). Various cortisol-regulated physiological processes depend on glucocorticoid receptor (GR), which is activated upon cortisol binding (20,21).…”

Section: Endocrine Factors and Metsmentioning

confidence: 99%

“…Cortisol regulates energy metabolism through gluconeogenesis, but also affects processes such as infl ammation (19,20). Various cortisol-regulated physiological processes depend on glucocorticoid receptor (GR), which is activated upon cortisol binding (20,21). On the pre-receptor level, cortisol action is additionally regulated by the intracellular enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD) (20,22,23) that comes in two isoforms: type 1 (11β-HSD1) and type 2 (11β-HSD2).…”

Section: Endocrine Factors and Metsmentioning

confidence: 99%

“…Various cortisol-regulated physiological processes depend on glucocorticoid receptor (GR), which is activated upon cortisol binding (20,21). On the pre-receptor level, cortisol action is additionally regulated by the intracellular enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD) (20,22,23) that comes in two isoforms: type 1 (11β-HSD1) and type 2 (11β-HSD2). Type 1 catalyses the conversion of the inactive form cortisone into active cortisol, while type 2 converts active cortisol into its inactive form cortisone to lower the levels of active glucocorticoid and to inhibit cortisol activity (22,24).…”

Section: Endocrine Factors and Metsmentioning

confidence: 99%

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Endocrine, Lifestyle, and Genetic Factors in the Development of Metabolic Syndrome

Slanovic-Kuzmanović

Kos

Domijan

2013

Archives of Industrial Hygiene and Toxicology

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Metabolic syndrome (MetS) is a chronic, multi-component disease characterised by central obesity, hyperglycaemia, dyslipidaemia, and hypertension. Since MetS leads to type 2 diabetes, cardiovascular disease, development of certain cancers, and eventually to premature death, it is not surprising that it draws the attention of scientists around the world. The aetiopathology of MetS is complex and still not fully understood. This review focuses on the role of endocrine factors such as cortisol and insulin in the development of MetS. It also takes a look at some of the contributing lifestyle and genetic factors as well as at the current knowledge about its treatment. Slanovic-Kuzmanović Z, et al. ENDOCRINE, LIFESTYLE, AND GENETIC RISK FACTORS FOR METS Arh Hig Rada Toksikol 2013;64:581-591 Metabolic syndrome (MetS) is a modern disease characterised by the clustering of abnormalities such as central obesity, high levels of fasting glucose and triglyceride, low levels of high-density lipoprotein (HDL), and hypertension (1, 2). The prevalence of MetS has been increasing over the past two decades (1), and recent studies (3-5) suggest that it has reached 25 % among the adults worldwide. Reports vary from 21.9 % in men and 16.8 % in women in north-eastern Italy, and 24.6 % in alcohol-dependent male patients in north India to 31.25 % in rural women from Bangladesh. A small study on salt intake with 92 participants in Croatia reports the prevalence of 31.5 % (6). Among obese adolescents and pubertal children, the prevalence of MetS could be around 15 %, judging by the reports of 14 % in Danish obese adolescents (7) and of 9.7 % to 41.2 % in obese pubertal children and 8.3 % to 34.2 % in obese prepubertal children in Spain (8). KEY WORDS: cardiovascular diseases, circadian rhythm, cortisol, hyperglycaemia, hypertension, insulin, MetS, type 2 diabetes

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LC–MS/MS method for the quantification of cortisol of hepatocellular carcinoma

Zhou,

Li,

Yin

et al. 2024

Biomedical Chromatography

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The imbalance of steroid hormones is closely related to the occurrence and development of hepatocellular carcinoma (HCC). However, most research has focused on steroid hormone receptors, and reports about the relationship between the serum concentration of cortisol and the development of HCC are rare. The aim of this research was to establish a simple, specific, sensitive and reliable liquid chromatography–mass spectrometry/mass spectrometry (LC–MS/MS) method for the quantitation of cortisol in human serum and to compare the level of cortisol in serum between 221 HCC patients and 183 healthy volunteers. The results showed that the correlation coefficients of the linear regression with a weighing factor of 1/x2 ranged from 0.9933 to 0.9984 over the range of 2–1,000 ng/ml. The inter‐ and intra‐day precision and accuracy were <10%. The matrix effect and recovery of cortisol were 94.9–102.5% and 96.3–99.8%, respectively. The concentration of cortisol in HCC patients was significantly higher than that in healthy volunteers (p < 0.05) and was not affected by sex, age, menopause or α‐fetoprotein (AFP) level. The present study reveals that elevated cortisol might promote the progression of HCC.

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11β-Hydroxysteroid dehydrogenase type 1 is an important regulator at the interface of obesity and inflammation

Cited by 96 publications

References 239 publications

HSD1 and AQP7 short-term gene regulation by cortisone in 3T3-L1 adipocytes

HSD1 and AQP7 short-term gene regulation by cortisone in 3T3-L1 adipocytes

Endocrine, Lifestyle, and Genetic Factors in the Development of Metabolic Syndrome

LC–MS/MS method for the quantification of cortisol of hepatocellular carcinoma

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