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Cortisol Conversion in Subjects with Central Adiposity1
Endocrinology, Division of Medical Sciences, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham, United Kingdom B15 2TH; the Regional Endocrine Laboratory, University Hospital Birmingham National Health Service Trust (P.M.S.C.), Birmingham, United Kingdom B29 6JD; and the Steroid Laboratory, Children’s Hospital Oakland Research Institute (C.H.L.S.), Oakland, California 94609-1809
Address all correspondence and requests for reprints to: Prof. Paul M. Stewart, Division of Medical Sciences, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham, United Kingdom B15 2TH. E-mail: p.m.stewart{at}bham.ac.uk
For a given body mass index (BMI), mortality is higher in patients with central compared to generalized obesity. Glucocorticoids play an important role in determining body fat distribution, but circulating cortisol concentrations are reported to be normal in obese patients. Our recent studies show enhanced conversion of inactive cortisone (E) to active cortisol (F) through the expression of 11ß-hydroxysteroid dehydrogenase type 1 (11ßHSD1) in cultured omental adipose stromal cells; the autocrine production of F may be a crucial factor in the pathogenesis of central obesity.
We have now analyzed F metabolism in subjects with BMIs between 20–25
kg/m2 (group A), 25–30 kg/m2 (group B), and
more than 30 kg/m2 (group C; n = 12 in each group; six
males and six premenopausal females; aged 23–44 yr). Glucose/insulin
were measured using a 75-g oral glucose tolerance test, and each
subject had total body and regional fat (scapular, waist, hip, and
thigh) quantified using dual energy x-ray absorptiometry. Urinary total
F metabolites (measured by gas chromatography/mass spectrometry) were
increased in subjects with obesity [group A, 11,176 ± 1,530
µg/24 h (mean ± SE); group C, 13,661 ±
1,444], although not significantly so (P = 0.08).
There was a significant reduction in the urinary tetrahydrocortisol
(THF) +/- 5
-THF/tetrahydrocortisone (THE) and the
cortol/cortolone ratio in obesity (group A vs. C,
1.06 ± 0.08 vs. 0.84 ± 0.04 and 0.41 ±
0.03 vs. 0.34 ± 0.03, respectively; both
P < 0.05). Urinary free F (UFF) excretion was
similar in all three groups, as was the UFF/urinary free E (UFE) ratio.
The 0900 h circulating F, E, and ACTH pre- and postovernight 1-mg
dexamethasone suppression values were similar in all three groups, but
a reduction in the generation of serum F from dexamethasone-suppressed
values after oral cortisone acetate (25 mg) was evident in both obese
groups [e.g. 546 ± 37 nmol/L in group A
vs. 412 ± 40 in group B (P <
0.05) and 388 ± 38 in group C (P < 0.01) 180
min post-E]. Insulin resistance was present in groups B and C, but
regression analysis revealed no relationship between F metabolites or
the THF+5-THF/THE ratio and insulin action (homeostasis model
assessment analysis and insulin values in the oral glucose tolerance
test). There was, however, a highly significant relationship between
the THF+5-THF/THE ratio and BMI (t = -3.44;
P < 0.01) and total body fat
(t = -2.27; P < 0.05).
Stepwise regression analyses indicated an inverse relationship between
THF+5-THF/THE and scapular and waist fat (t =
-2.25; P = 0.03) and a direct relationship with
hip and thigh fat (t = 2.42; P
= 0.02) in both sexes.
The fall in the THF+5-THF/THE ratio but unchanged UFF/UFE ratio
together with impaired F concentrations after oral E indicates
inhibition of 11ßHSD1 in subjects with obesity. This results in an
increased MCR for F, explaining the increased F secretion rate in
obesity in the face of normal circulating F concentrations. 11ßHSD1
activity is highly related to body fat distribution, with android or
central obesity, but not gynoid obesity, associated with reduced
activity in both sexes. This reduction in 11ßHSD1 activity raises new
questions as to the primary role of 11ßHSD1 in the pathogenesis of
insulin resistance and central obesity.
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N. Draper, S. M. Echwald, G. G. Lavery, E. A. Walker, R. Fraser, E. Davies, T. I. A. Sorensen, A. Astrup, J. Adamski, M. Hewison, et al. Association Studies between Microsatellite Markers within the Gene Encoding Human 11{beta}-Hydroxysteroid Dehydrogenase Type 1 and Body Mass Index, Waist to Hip Ratio, and Glucocorticoid Metabolism J. Clin. Endocrinol. Metab., November 1, 2002; 87(11): 4984 - 4990. [Abstract] [Full Text] [PDF]
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E. Rask, B. R. Walker, S. Soderberg, D. E. W. Livingstone, M. Eliasson, O. Johnson, R. Andrew, and T. Olsson Tissue-Specific Changes in Peripheral Cortisol Metabolism in Obese Women: Increased Adipose 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Activity J. Clin. Endocrinol. Metab., July 1, 2002; 87(7): 3330 - 3336. [Abstract] [Full Text] [PDF]
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P. G. McTernan, L. A. Anderson, A. J. Anwar, M. C. Eggo, J. Crocker, A. H. Barnett, P. M. Stewart, and S. Kumar Glucocorticoid Regulation of P450 Aromatase Activity in Human Adipose Tissue: Gender and Site Differences J. Clin. Endocrinol. Metab., March 1, 2002; 87(3): 1327 - 1336. [Abstract] [Full Text] [PDF]
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J. W. Tomlinson, N. Draper, J. Mackie, A. P. Johnson, G. Holder, P. Wood, and P. M. Stewart Absence of Cushingoid Phenotype in a Patient with Cushing's Disease due to Defective Cortisone to Cortisol Conversion J. Clin. Endocrinol. Metab., January 1, 2002; 87(1): 57 - 62. [Abstract] [Full Text] [PDF]
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R. Pasquali, B. Ambrosi, D. Armanini, F. Cavagnini, E. D. Uberti, G. Del Rio, G. de Pergola, M. Maccario, F. Mantero, M. Marugo, et al. Cortisol and ACTH Response to Oral Dexamethasone in Obesity and Effects of Sex, Body Fat Distribution, and Dexamethasone Concentrations: A Dose-Response Study J. Clin. Endocrinol. Metab., January 1, 2002; 87(1): 166 - 175. [Abstract] [Full Text] [PDF]
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R. Andrew, K. Smith, G. C. Jones, and B. R. Walker Distinguishing the Activities of 11{beta}-Hydroxysteroid Dehydrogenases in Vivo Using Isotopically Labeled Cortisol J. Clin. Endocrinol. Metab., January 1, 2002; 87(1): 277 - 285. [Abstract] [Full Text] [PDF]
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D. S. Jessop, M. F. Dallman, D. Fleming, and S. L. Lightman Resistance to Glucocorticoid Feedback in Obesity J. Clin. Endocrinol. Metab., September 1, 2001; 86(9): 4109 - 4114. [Abstract] [Full Text] [PDF]
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A. Johansson, R. Andrew, H. Forsberg, K. Cederquist, B. R. Walker, and T. Olsson Glucocorticoid Metabolism and Adrenocortical Reactivity to ACTH in Myotonic Dystrophy J. Clin. Endocrinol. Metab., September 1, 2001; 86(9): 4276 - 4283. [Abstract] [Full Text] [PDF]
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J. W. Tomlinson, J. Moore, M. S. Cooper, I. Bujalska, M. Shahmanesh, C. Burt, A. Strain, M. Hewison, and P. M. Stewart Regulation of Expression of 11{beta}-Hydroxysteroid Dehydrogenase Type 1 in Adipose Tissue: Tissue-Specific Induction by Cytokines Endocrinology, May 1, 2001; 142(5): 1982 - 1989. [Abstract] [Full Text]
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J. R. Seckl and B. R. Walker Minireview: 11{beta}-Hydroxysteroid Dehydrogenase Type 1-- A Tissue-Specific Amplifier of Glucocorticoid Action Endocrinology, April 1, 2001; 142(4): 1371 - 1376. [Abstract] [Full Text]
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P. S. Brereton, R. R. van Driel, F. b. H. Suhaimi, K. Koyama, R. Dilley, and Z. Krozowski Light and Electron Microscopy Localization of the 11{beta}-Hydroxysteroid Dehydrogenase Type I Enzyme in the Rat Endocrinology, April 1, 2001; 142(4): 1644 - 1651. [Abstract] [Full Text]
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P. Ferrari Author's Response: In Vivo Measurements of Renal 11{beta}-Hydroxysteroid Dehydrogenase Type 2 Activity J. Clin. Endocrinol. Metab., December 1, 2000; 85(12): 4922 - 4923. [Full Text]
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M. Quinkler, W. Oelkers, and S. Diederich In Vivo Measurement of Renal 11{beta}-Hydroxysteroid Dehydrogenase Type 2 Activity J. Clin. Endocrinol. Metab., December 1, 2000; 85(12): 4921a - 4922. [Full Text]
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V. Vicennati and R. Pasquali Abnormalities of the Hypothalamic-Pituitary-Adrenal Axis in Nondepressed Women with Abdominal Obesity and Relations with Insulin Resistance: Evidence for a Central and a Peripheral Alteration J. Clin. Endocrinol. Metab., November 1, 2000; 85(11): 4093 - 4098. [Abstract] [Full Text]
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 L. C. Morin-Papunen, I. Vauhkonen, R. M. Koivunen, A. Ruokonen, and J. S. Tapanainen Insulin sensitivity, insulin secretion, and metabolic and hormonal parameters in healthy women and women with polycystic ovarian syndrome Hum. Reprod., June 1, 2000; 15(6): 1266 - 1274. [Abstract] [Full Text] [PDF]
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A. A. Toogood, N. F. Taylor, S. M. Shalet, and J. P. Monson Modulation of Cortisol Metabolism by Low-Dose Growth Hormone Replacement in Elderly Hypopituitary Patients J. Clin. Endocrinol. Metab., April 1, 2000; 85(4): 1727 - 1730. [Abstract] [Full Text]
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D. E. W. Livingstone, G. C. Jones, K. Smith, P. M. Jamieson, R. Andrew, C. J. Kenyon, and B. R. Walker Understanding the Role of Glucocorticoids in Obesity: Tissue-Specific Alterations of Corticosterone Metabolism in Obese Zucker Rats Endocrinology, February 1, 2000; 141(2): 560 - 563. [Abstract] [Full Text] [PDF]
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M. J. J. Finken, R. C. Andrews, R. Andrew, and B. R. Walker Cortisol Metabolism in Healthy Young Adults: Sexual Dimorphism in Activities of A-Ring Reductases, but not 11{beta}-Hydroxysteroid Dehydrogenases J. Clin. Endocrinol. Metab., September 1, 1999; 84(9): 3316 - 3321. [Abstract] [Full Text]
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N. M. Morton, M. C. Holmes, C. Fievet, B. Staels, A. Tailleux, J. J. Mullins, and J. R. Seckl Improved Lipid and Lipoprotein Profile, Hepatic Insulin Sensitivity, and Glucose Tolerance in 11beta -Hydroxysteroid Dehydrogenase Type 1 Null Mice J. Biol. Chem., October 26, 2001; 276(44): 41293 - 41300. [Abstract] [Full Text] [PDF]
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