ArticleThe Journal of endocrinology2008
A novel selective 11beta-hydroxysteroid dehydrogenase type 1 inhibitor prevents human adipogenesis.
Article in The Journal of endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 84 citations in OpenAlex.
- Hair cortisol as a complementary marker of chronic glucocorticoid exposure in mild autonomous cortisol secretion.BMC endocrine disorders · 2026Article
- Weak Noncovalent Interactions in Three Closely Related Adamantane-Linked 1,2,4-TriazoleMolecules (Basel, Switzerland) · 2022Article
- 11β-Hydroxysteroid Dehydrogenase Type 1 as a Potential Treatment Target in Cardiovascular Diseases.Journal of clinical medicine · 2022Review
- Equisetin is an anti-obesity candidate through targeting 11Acta pharmaceutica Sinica. B · 2022Article
- Effects ofFrontiers in bioengineering and biotechnology · 2022Article
- Structural Insights and Docking Analysis of Adamantane-Linked 1,2,4-Triazole Derivatives as Potential 11β-HSD1 Inhibitors.Molecules (Basel, Switzerland) · 2021Article
- Selective Inhibition of 11β-Hydroxysteroid Dehydrogenase Type 1 Attenuates High-Fat Diet-Induced Hepatic Steatosis in Mice.Drug design, development and therapy · 2021Article
- Endogenous Glucocorticoid Metabolism in Bone: Friend or Foe.Frontiers in endocrinology · 2021Review
- Crystal structure, Hirshfeld surface analysis and DFT studies of 5-(adamantan-1-yl)-3-[(4-chlorobenzyl)sulfanyl]-4-methyl-4H-1,2,4-triazole, a potential 11β-HSD1 inhibitor.Scientific reports · 2019Article
- An inhibitor of 11-β hydroxysteroid dehydrogenase type 1 (PF915275) alleviates nonylphenol-induced hyperadrenalism and adiposity in rat and human cells.BMC pharmacology & toxicology · 2018Article
- MicroRNA-130b attenuates dexamethasone-induced increase of lipid accumulation in porcine preadipocytes by suppressing PPAR-γ expression.Oncotarget · 2017Article
- 11β-Hydroxysteroid dehydrogenase type 1 within muscle protects against the adverse effects of local inflammation.The Journal of pathology · 2016Article
- Glucocorticoids and 11β-HSD1 are major regulators of intramyocellular protein metabolism.The Journal of endocrinology · 2016Article
- Short-term efficacy of recombinant human GH therapy in cured acromegaly patients with GH deficiency: a single-center experience.Endocrine connections · 2015Article
- Transgenic overexpression of hexose-6-phosphate dehydrogenase in adipose tissue causes local glucocorticoid amplification and lipolysis in male mice.American journal of physiology. Endocrinology and metabolism · 2014Article
- Mechanisms of glucocorticoid-induced insulin resistance: focus on adipose tissue function and lipid metabolism.Endocrinology and metabolism clinics of North America · 2014Review
- Irregularities in glucose metabolism induced by stress and high-calorie diet can be attenuated by glycyrrhizic acid.International journal of physiology, pathophysiology and pharmacology · 2014Article
- Dehydroepiandrosterone exerts antiglucocorticoid action on human preadipocyte proliferation, differentiation, and glucose uptake.American journal of physiology. Endocrinology and metabolism · 2013Article
- Human but not mouse adipogenesis is critically dependent on LMO3.Cell metabolism · 2013Article
- 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action.Physiological reviews · 2013Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Glucocorticoid excess increases fat mass, preferentially within omental depots; yet circulating cortisol concentrations are normal in most patients with metabolic syndrome (MS). At a pre-receptor level, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) activates cortisol from cortisone locally within adipose tissue, and inhibition of 11beta-HSD1 in liver and adipose tissue has been proposed as a novel therapy to treat MS by reducing hepatic glucose output and adiposity. Using a transformed human subcutaneous preadipocyte cell line (Chub-S7) and human primary preadipocytes, we have defined the role of glucocorticoids and 11beta-HSD1 in regulating adipose tissue differentiation. Human cells were differentiated with 1.0 microM cortisol (F), or cortisone (E) with or without 100 nM of a highly selective 11beta-HSD1 inhibitor PF-877423. 11beta-HSD1 mRNA expression increased across adipocyte differentiation (P<0.001, n=4), which was paralleled by an increase in 11beta-HSD1 oxo-reductase activity (from nil on day 0 to 5.9+/-1.9 pmol/mg per h on day 16, P<0.01, n=7). Cortisone enhanced adipocyte differentiation; fatty acid-binding protein 4 expression increased 312-fold (P<0.001) and glycerol-3-phosphate dehydrogenase 47-fold (P<0.001) versus controls. This was abolished by co-incubation with PF-877423. In addition, cellular lipid content decreased significantly. These findings were confirmed in the primary cultures of human subcutaneous preadipocytes. The increase in 11beta-HSD1 mRNA expression and activity is essential for the induction of human adipogenesis. Blocking adipogenesis with a novel and specific 11beta-HSD1 inhibitor may represent a novel approach to treat obesity in patients with MS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.