ArticleEndocrinology2017
11β-HSD1 Modulates the Set Point of Brown Adipose Tissue Response to Glucocorticoids in Male Mice.
Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Human Adipose Tissue 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition Without Tachyphylaxis by Clofutriben, a Pseudo-Irreversible Enzyme Inhibitor.Clinical and translational science · 2025Article
- Glucocorticoid excess alters metabolic rate and substrate utilisation via 11β-HSD1.The Journal of endocrinology · 2024Article
- 11β hydroxysteroid dehydrogenase type 1 transgenic mesenchymal stem cells attenuate inflammation in models of sepsis.Frontiers in bioengineering and biotechnology · 2024Article
- Standardized In Vitro Models of Human Adipose Tissue Reveal Metabolic Flexibility in Brown Adipocyte Thermogenesis.Endocrinology · 2023Article
- Impaired alveolar macrophage 11β-hydroxysteroid dehydrogenase type 1 reductase activity contributes to increased pulmonary inflammation and mortality in sepsis-related ARDS.Frontiers in immunology · 2023Article
- 11β-HSD1 contributes to age-related metabolic decline in male mice.The Journal of endocrinology · 2022Article
- Sexual Dimorphism in Adipose-Hypothalamic Crosstalk and the Contribution of Aryl Hydrocarbon Receptor to Regulate Energy Homeostasis.International journal of molecular sciences · 2022Review
- Chronic glucocorticoid exposure causes brown adipose tissue whitening, alters whole-body glucose metabolism and increases tissue uncoupling protein-1.Physiological reports · 2022Article
- Adipose tissue aging: mechanisms and therapeutic implications.Cell death & disease · 2022Review
- Mass Cytometry Study on Hepatic Fibrosis and Its Drug-Induced Recovery Using Mouse Peripheral Blood Mononuclear Cells.Frontiers in immunology · 2022Article
- Genomic and Non-Genomic Actions of Glucocorticoids on Adipose Tissue Lipid Metabolism.International journal of molecular sciences · 2021Review
- HAND2 is a novel obesity-linked adipogenic transcription factor regulated by glucocorticoid signalling.Diabetologia · 2021Article
- Sex Differences in Brown Adipose Tissue Function: Sex Hormones, Glucocorticoids, and Their Crosstalk.Frontiers in endocrinology · 2021Review
- Mechanisms Underlying the Regulation of Mitochondrial Respiratory Chain Complexes by Nuclear Steroid Receptors.International journal of molecular sciences · 2020Review
- The glucocorticoid receptor in brown adipocytes is dispensable for control of energy homeostasis.EMBO reports · 2019Article
- Glucocorticoid Receptor and Adipocyte Biology.Nuclear receptor research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Glucocorticoids (GCs) are potent regulators of energy metabolism. Chronic GC exposure suppresses brown adipose tissue (BAT) thermogenic capacity in mice, with evidence for a similar effect in humans. Intracellular GC levels are regulated by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity, which can amplify circulating GC concentrations. Therefore, 11β-HSD1 could modulate the impact of GCs on BAT function. This study investigated how 11β-HSD1 regulates the molecular architecture of BAT in the context of GC excess and aging. Circulating GC excess was induced in 11β-HSD1 knockout (KO) and wild-type mice by supplementing drinking water with 100 μg/mL corticosterone, and the effects on molecular markers of BAT function and mitochondrial activity were assessed. Brown adipocyte primary cultures were used to examine cell autonomous consequences of 11β-HSD1 deficiency. Molecular markers of BAT function were also examined in aged 11β-HSD1 KO mice to model lifetime GC exposure. BAT 11β-HSD1 expression and activity were elevated in response to GC excess and with aging. 11β-HSD1 KO BAT resisted the suppression of uncoupling protein 1 (UCP1) and mitochondrial respiratory chain subunit proteins normally imposed by GC excess. Furthermore, brown adipocytes from 11β-HSD1 KO mice had elevated basal mitochondrial function and were able to resist GC-mediated repression of activity. BAT from aged 11β-HSD1 KO mice showed elevated UCP1 protein and mitochondrial content, and a favorable profile of BAT function. These data reveal a novel mechanism in which increased 11β-HSD1 expression, in the context of GC excess and aging, impairs the molecular and metabolic function of BAT.
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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.