The DOI matches its Crossref record; 148 of the 148 references it cites were found in a registry or an index.
Glucocorticoids and 11beta-Hydroxysteroid Dehydrogenase in Adipose Tissue
Open accessAbstract
The highly prevalent metabolic syndrome (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, along with abdominal obesity) resembles Cushing's syndrome. However, in simple obesity, plasma cortisol levels are not elevated. 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), at least in mature adipocytes and hepatocytes, converts inactive circulating 11-keto steroids into active glucocorticoids, amplifying local glucocorticoid action. 11beta-HSD1 is elevated in adipose tissue in obese humans and rodents, suggesting that adipose tissue glucocorticoid excess may explain the conundrum. Indeed, transgenic mice overexpressing 11beta-HSD1 in adipose tissue faithfully replicate the metabolic syndrome. Conversely, 11beta-HSD1(-/-) mice resist the metabolic consequences of stress and high-fat feeding via insulin sensitisation and other advantageous effects in the liver and adipose tissue. Adipose 11beta-HSD1 deficiency contributes to a protective metabolic phenotype, supporting its role as a therapeutic target for the metabolic syndrome.
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Citations
Cites
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Cited by
Sorted by citations
The Molecular Biology, Biochemistry, and Physiology of Human Steroidogenesis and Its Disorders
Miller, W. L., & Auchus, R. J. (2011) · Endocrine Reviews · doi:10.1210/er.2010-0013 · Cited by 2,458
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“Increased tissue sensitivity to glucocorticoids has gained significant attention with the discovery of 11-β hydroxysteroid dehydrogenase (11β HSD), an enzyme that regulates glucocorticoid access to the receptors in peripheral and brain tissue and converts inactive glucocorticoids such as cortisone to active glucocorti…”
BackgroundGlucocorticoids, prenatal stress and the programming of disease
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Self-citationHypoxia and Adipose Tissue Function and Dysfunction in Obesity
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Metadata
- Authors
- Seckl, J. R.
- Affiliations
- Western General Hospital (GB)
- Corresponding author
- Seckl, J. R.
- ORCID
- Seckl, J. R.
- Venue
- Recent Progress in Hormone Research
- Publisher
- The Endocrine Society
- Published
- 2004-01-01
- Volume
- 59
- Issue
- 1
- Pages
- 359-393
- ISSN
- 0079-9963 (ISSN-L)
- OpenAlex
- W2129008449
- Semantic Scholar
- 4c2b062bc15435b616374945d43d7e9a6e33c792
- Cited by
- 239
- References
- 147
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 4 · 2020: 5 · 2019: 6 · 2018: 7 · 2017: 5 · 2016: 1 · 2015: 9 · 2014: 11 · 2013: 15 · 2012: 18
- FWCI
- 3.34
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- Recent Progress in Hormone Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- British Heart Foundation
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- 11β-hydroxysteroid dehydrogenase type 1, adipose tissue, glucocorticoids, metabolic syndrome, obesity, insulin resistance, type 2 diabetes, 11-keto steroids, transgenic mice, high-fat feeding, therapeutic target
- MeSH terms
- Adipose Tissue, Adrenal Glands, Animals, Glucocorticoids, Humans, Hypothalamus, Liver, Mice, Transgenic, Obesity, Pituitary Gland, Mice, Knockout, Metabolic Syndrome, 11-beta-Hydroxysteroid Dehydrogenases, Mice
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