A switch in dehydrogenase to reductase activity of 11 beta-hydroxysteroid dehydrogenase type 1 upon differentiation of human omental adipose stromal cells.
Bujalska IJ., Walker EA., Hewison M., Stewart PM.
Prospective Study with a reported sample of 17 on Hip, published in J Clin Endocrinol Metab (2002) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Prospective Study
- Journal
- J Clin Endocrinol Metab (2002)
- Country
- United States
- Reported sample size
- 17
- Source database
- PubMed
- PMID
- 11889189
- DOI
- 10.1210/jcem.87.3.8301
Abstract (original English)
As exemplified in patients with Cushing's syndrome, glucocorticoids play an important role in regulating adipose tissue distribution and function, but circulating cortisol concentrations are normal in most patients with obesity. However, human omental adipose stromal cells (ASCs) can generate glucocorticoid locally through the expression of the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) type 1 (11 beta-HSD1), which, in intact cells, has been considered to be an oxoreductase, converting inactive cortisone (E) to cortisol (F). Locally produced F can induce ASC differentiation, but the relationship between 11 beta-HSD1 expression and adipocyte differentiation is unknown. Primary cultures of paired omental (om) and sc ASC and adipocytes were prepared from 17 patients undergoing elective abdominal surgery and cultured for up to 14 d. Expression and activity of 11 beta-HSD isozymes were analyzed together with early (lipoprotein lipase) and terminal (glycerol 3 phosphate dehydrogenase) markers of adipocyte differentiation. On d 1 of culture, 11 beta-HSD1 activity in intact om ASCs exceeded oxoreductase activity in every patient (78.9 +/- 24.9 vs. 15.8 +/- 3.7 [mean +/- SE] pmol/mg per hour, P < 0.001), and in sc ASCs, relative activities were similar (40.6 +/- 12.2 vs. 36.9 +/- 8.8). Conversely, in freshly isolated om adipocytes, reductase activity exceeded dehydrogenas
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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