Does central obesity reflect “Cushing's disease of the omentum”?
@article{Bujalska1997DoesCO, title={Does central obesity reflect “Cushing's disease of the omentum”?}, author={Iwona J. Bujalska and Sudhesh Kumar and Paul M Stewart}, journal={The Lancet}, year={1997}, volume={349}, pages={1210-1213} }
775 Citations
Tissue-specific changes in peripheral cortisol metabolism in obese women: increased adipose 11beta-hydroxysteroid dehydrogenase type 1 activity.
- Medicine, BiologyThe Journal of clinical endocrinology and metabolism
- 2002
In obese females increased reactivation of glucocorticoids in fat may contribute to the characteristics of the metabolic syndrome and alterations in cortisol metabolism may be a basis for novel therapeutic strategies to reduce obesity-related complications.
Weight loss increases 11beta-hydroxysteroid dehydrogenase type 1 expression in human adipose tissue.
- Medicine, BiologyThe Journal of clinical endocrinology and metabolism
- 2004
The effects of significant weight loss on cortisol metabolism and adipose tissue 11betaHSD1 expression after 10-wk ingestion of a very low calorie diet in 12 obese patients are determined and inhibition of 11beta HSD1 may be a novel, therapeutic strategy for insulin sensitization.
Obesity and corticosteroids: 11β-Hydroxysteroid type 1 as a cause and therapeutic target in metabolic disease
- Biology, MedicineMolecular and Cellular Endocrinology
- 2010
11β-Hydroxysteroid Dehydrogenase Type 1 and Obesity
- Biology, Medicine
- 2007
Tissue-specific dysregulation of glucocorticoids occurs in simple obesity, with increased 11α-HSD1 activity in subcutaneous adipose tissue and decreased activity in the liver.
Expression of 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue is not increased in human obesity.
- Biology, MedicineThe Journal of clinical endocrinology and metabolism
- 2002
It is hypothesized that the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), by converting inactive cortisone to active cortisol in adipose tissue, might be an important autocrine regulator of fat mass.
Characterisation of 11β-hydroxysteroid dehydrogenase 1 in human orbital adipose tissue: a comparison with subcutaneous and omental fat
- Biology, MedicineThe Journal of endocrinology
- 2007
Features of the GC metabolic pathways in normal human OF depot are described and compared with subcutaneous (SC) and OM depots and Orbital adipocytes are smaller, less differentiated, and express low levels of 11β-HSD1 but abundant GRα compared with SC and OM.
11β-hydroxysteroid dehydrogenase type 1 is not over expressed in cushing’s syndrome adipose depots
- Medicine, Biology
- 2014
Chronic hypercortisolism, as seen in CS, does not result in upregulation of 11β-HSD1 expression in adipose depots, in contrast with in vitro observations, which may suggest a protective mechanism, since 11 β- HSD1 is emerging as a key component in homeostatic adaptation, rather than the cause of visceral obesity.
The Role of 11 β-Hydroxysteroid Dehydrogenase in Central Obesity and Osteoporosis
- Biology, MedicineEndocrine research
- 2000
Investigation of the effect of various factors present within the adipocyte microenvironment for their effects on 11β-HSD1 expression finds the action of growth factors and cytokines on glucocorticoid sensitive tissues such as adipose tissue and bone may be mediated by modulation of local glucoc Corticoid metabolism at a pre-receptor level.
11Β-Hydroxysteroid Dehydrogenase Type 1 and Obesity
- Biology, Medicine
- 2008
Transgenic mice overexpressing 11Β -HSD1 in adipose tissue or liver exhibited improved glucose tolerance, a ‘cardioprotective’ lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding, corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
Cortisol metabolism in human obesity: impaired cortisone-->cortisol conversion in subjects with central adiposity.
- Medicine, BiologyThe Journal of clinical endocrinology and metabolism
- 1999
F metabolism in subjects with BMIs between 20-25 kg/m2 ( group A), 25-30 kg/ m2 (group B), and more than 30kg/m3 (group C) is analyzed, finding an increased MCR for F results in an increased F secretion rate in obesity in the face of normal circulating F concentrations.
References
SHOWING 1-10 OF 23 REFERENCES
The hypothalamic-pituitary-adrenal axis in obese women with different patterns of body fat distribution.
- Medicine, BiologyThe Journal of clinical endocrinology and metabolism
- 1993
It is suggested that obese women with A-BFD may have hyperactivity of the hypothalamic-pituitary-adrenal axis and this abnormality could be central in origin, due to hypersecretion of CRF or ACTH; alternatively, it could represent an adaptive phenomenon secondary to a state of functional cortisol resistance.
Hypertension in the syndrome of apparent mineralocorticoid excess due to mutation of the 11β-hydroxysteroid dehydrogenase type 2 gene
- Biology, MedicineThe Lancet
- 1996
Metabolic Implications of Body Fat Distribution
- Medicine, BiologyDiabetes Care
- 1991
It is hypothesized that free fatty acids and testosterone might provide a background not only to a defense reaction and primary hypertension, suggested previously, but also to a defeat reaction, which contributes to an endocrine aberration leading to metabolic aberrations and visceral fat accumulation, which in turn leads to disease.
11β‐Hydroxysteroid dehydrogenase: implications for clinical medicine
- Medicine, Biology
- 1996
Further understanding of the pathogenesis of AME, and studies on the enzymology of 11 -HSD in the interim, have yielded considerable insight into the mechanisms of corticosteroid hormone action in normal physiology and in disease states.
Muscle and adipose tissue morphology and metabolism in Cushing's syndrome.
- Medicine, BiologyThe Journal of clinical endocrinology and metabolism
- 1988
The enlargement of abdominal fat depots in women with Cushing's syndrome is at least partially due to elevated adipocyte lipoprotein lipase activity and low lipolytic activity, and the abnormal muscle fiber composition might be caused by the corticosteroid excess.
LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR
- Biology, MedicineThe Lancet
- 1988
11 beta-hydroxysteroid dehydrogenase is an exclusive 11 beta- reductase in primary cultures of rat hepatocytes: effect of physicochemical and hormonal manipulations.
- Biology, MedicineEndocrinology
- 1995
Conditions for primary culture of adult rat hepatocytes that maintain high 11 beta HSR-1 messenger RNA expression are defined, which will allow investigation of the control of 11 beta-reductase activity and its implications for glucocorticoid-regulated hepatic functions.
Effect of glucocorticosteroid treatment on glucocorticoid receptor expression in human adipocytes.
- Biology, MedicineThe Journal of clinical endocrinology and metabolism
- 1995
It is shown that glucocorticoids modulate human adipose metabolism by altering the expression of regulatory proteins at various mRNA and post-mRNA levels and selectively increases beta 2-adrenoceptor density in sc fat cells of healthy individuals.
Cloning and tissue distribution of the human 1 lβ-hydroxysteroid dehydrogenase type 2 enzyme
- BiologyMolecular and Cellular Endocrinology
- 1994
Detection of human 11β-hydroxysteroid dehydrogenase isoforms using reverse-transcriptase-polymerase chain reaction and localization of the type 2 isoform to renal collecting ducts
- Biology, MedicineMolecular and Cellular Endocrinology
- 1995