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}
}
Tissue-specific changes in peripheral cortisol metabolism in obese women: increased adipose 11beta-hydroxysteroid dehydrogenase type 1 activity.
TLDR
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.
TLDR
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.
11β-Hydroxysteroid Dehydrogenase Type 1 and Obesity
TLDR
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.
TLDR
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
TLDR
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
TLDR
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
TLDR
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
TLDR
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.
TLDR
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.
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