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Novel Adipose Tissue–Mediated Resistance to Diet-Induced Visceral Obesity in 11β-Hydroxysteroid Dehydrogenase Type 1–Deficient Mice
Open accessAbstract
The metabolic syndrome (visceral obesity, insulin resistance, type 2 diabetes, and dyslipidemia) resembles Cushing’s Syndrome, but without elevated circulating glucocorticoid levels. An emerging concept suggests that the aberrantly elevated levels of the intracellular glucocorticoid reamplifying enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) found in adipose tissue of obese humans and rodents underlies the phenotypic similarities between idiopathic and “Cushingoid” obesity. Transgenic overexpression of 11β-HSD-1 in adipose tissue reproduces a metabolic syndrome in mice, whereas 11β-HSD-1 deficiency or inhibition has beneficial metabolic effects, at least on liver metabolism. Here we report novel protective effects of 11β-HSD-1 deficiency on adipose function, distribution, and gene expression in vivo in 11β-HSD-1 nullizygous (11β-HSD-1−/−) mice. 11β-HSD-1−/− mice expressed lower resistin and tumor necrosis factor-α, but higher peroxisome proliferator–activated receptor-γ, adiponectin, and uncoupling protein-2 mRNA levels in adipose, indicating insulin sensitization. Isolated 11β-HSD-1−/− adipocytes exhibited higher basal and insulin-stimulated glucose uptake. 11β-HSD-1−/− mice also exhibited reduced visceral fat accumulation upon high-fat feeding. High-fat–fed 11β-HSD-1−/− mice rederived onto the C57BL/6J strain resisted diabetes and weight gain despite consuming more calories. These data provide the first in vivo evidence that adipose 11β-HSD-1 deficiency beneficially alters adipose tissue distribution and function, complementing the reported effects of hepatic 11β-HSD-1 deficiency or inhibition.
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“These include increased production of inflammatory cytokines, 35,36 plasminogen activator inhibitor-1, 37 and other bioactive products 38 -40 ; at the same time the potentially protective adipokine, adiponectin, is reduced.41,42”
From Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement (2005) · cites this paper as [38]
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Metadata
- Authors
- Morton, N. M., Paterson, J. M., Masuzaki, H., Holmes, M. C., Staels, B., Fievet, C., Walker, B. R., Flier, J. S., Mullins, J. J., & Seckl, J. R.
- Affiliations
- Western General Hospital (GB)
- University of Edinburgh (GB)
- Kyoto University (JP)
- Inserm (FR)
- Département d’ Athérosclérose,U.545 INSERM, Institut Pasteur de Lille, Lille, France
- Beth Israel Deaconess Medical Center (US)
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2004-04-01
- Volume
- 53
- Issue
- 4
- Pages
- 931-938
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2154972651
- Cited by
- 512
- References
- 49
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 9 · 2023: 6 · 2022: 9 · 2021: 9 · 2020: 5 · 2019: 10 · 2018: 10 · 2017: 12 · 2016: 21 · 2015: 19 · 2014: 24 · 2013: 35 · 2012: 37
- FWCI
- 32.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (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 › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- 11β-hydroxysteroid dehydrogenase type 1, visceral obesity, adipose tissue, metabolic syndrome, insulin resistance, resistin, TNF-α, PPARγ, adiponectin, UCP2, insulin-stimulated glucose uptake, high-fat diet, body fat distribution, type 2 diabetes
- MeSH terms
- Uncoupling Protein 2, Adipose Tissue, Animals, Blood Glucose, Body Temperature, Body Weight, Cholesterol, Diet, Gene Expression Regulation, Glucose Tolerance Test, Insulin, Ion Channels, Male, Obesity, Transcription Factors, Triglycerides, Adipocytes, Receptors, Cytoplasmic and Nuclear, Mice, Knockout, Mitochondrial Proteins, Membrane Transport Proteins, 11-beta-Hydroxysteroid Dehydrogenase Type 1, Mice
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