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Original Studies |
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
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Abstract |
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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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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The aim of this study was to evaluate F metabolism in patients with varying degrees of obesity.
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Subjects and Methods |
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-THF, tetrahydrocortisone (THE),
cortols, cortolones, and free F], urinary free F (UFF)/urinary
free E (UFE), THF+5-THF/THE, cortols/cortolones, THF/5-THF, and
etiocholanolone/androsterone. On day 2, an oral glucose tolerance test was undertaken, giving 75 g oral glucose to a fasted subject at 0900 h and measuring plasma glucose and insulin at 30-min intervals for 120 min; samples were collected on ice and centrifuged immediately, and the plasma was stored before analysis.
At 2300 h on day 2, subjects were given 1 mg dexamethasone, orally, to suppress endogenous F production. All subjects reattended at 0900 h the following morning, and after baseline 0900 h measurements of F and ACTH, cortisone acetate (25 mg) was given orally. Serum F and cortisone acetate were then measured at 30- to 60-min intervals for 240 min as previously reported (24).
Plasma glucose, serum triglycerides, and cholesterol were measured using standard laboratory methods (Instrumentation Laboratory, Warrington, UK). F was measured with an automated competitive chemiluminescent assay on the ACS 180 (Chiron Diagnostics, Halstead, UK), with interassay coefficients of variation (CVs) of less than 10% over the concentration range of 53–944 nmol/L. The 0900 h reference range is quoted at 180–550 nmol/L. E was analyzed by RIA, using antiserum N-137 and 21-acetyl-cortisone-3CMO-histamine[125I] tracer, as previously reported (25). ACTH was measured using an immunoradiometric assay (Nichols Institute Diagnostics Ltd., Saffron Walden, UK), with interassay CVs of less than 15% from 8.4–1333 ng/L. The 0900 h reference range is 9–52 ng/L. Urinary free F was measured by a dichloromethane extraction RIA, with interassay CVs of less than 16% over the range of 153–798 nmol/L. Serum free T4, free T3, and TSH were measured by automated luminescent immunoassays on the ACS180 (Chiron Diagnostics), with interassay CVs of less than 12% over the ranges of 6.2–81 pmol/L, 2.5–20 pmol/L, and 0.3–39 mIU/L, respectively. Insulin was measured using an immunoenzymometric assay with no significant cross-reactivity with intact or partially processed proinsulins (Medgenix, Lifescreen, Watford, UK), calibrated against International Reference Preparation 66/304. Interassay CVs were less than 8% over the concentration range of 95–580 pmol/L. Insulin sensitivity was derived from fasting glucose and insulin data, using the homeostasis model assessment (HOMA) mathematical model (26). Insulin sensitivity (HOMA -%S) was expressed as percentage relative to a lean healthy reference population; insulin resistance was inferred from values less than 100%.
Whole body DEXA measurements were performed with a total body scanner (Lunar DPX-L, Lunar Radiation Corp., Madison, WI), and total body fat was recorded. Regions of the body were delineated using previously described landmarks, and regional fat was calculated for subscapular, waist, hip, and thigh regions (27). Waist region was defined within a box area between the upper part of D12 and the iliac crest and subscapular region defined by the same box height immediately above D12. The hip region was the same box height, positioned so that its upper border passed through the superior points of the inner pelvis, and the thigh region was the same box height, with its superior border at the level of the inferior border of the hip region. In each case the sides of the box were lateral to any trunk tissue. The precision of total fat mass measures in terms of CV were less than 3%, and CVs for the regional fat analyses were less than 5%. Regional fat data were expressed as a percentage of the total body fat.
Results are expressed as the mean ± SE. Statistical analyses among the three groups and, where appropriate, between males and females, was undertaken using Student’s unpaired t test. Stepwise regression and regression analysis were undertaken to define predictive variables. In both cases a Minitab Statistics package was used (version 10.5 for Windows).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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).
Serum F concentrations after a 1-mg overnight dexamethasone suppression
test were similar in all three groups (27.9 ± 2.0, 27 ±
2.4, and 24.3 ± 1.3 nmol/L, respectively, in groups A, B, and C),
as were free T4, free T3, and TSH. Basal and
peak glucose values after glucose ingestion were also similar in all
groups, although the two obese groups (B and C) showed evidence of
hyperinsulinemia and an exaggerated insulin response to glucose
ingestion. When expressed as HOMA -%S, groups B and C were
significantly more insulin resistant than group A (Table 1). Systolic
blood pressure was generally increased with increasing obesity,
although absolute values did not reach statistical significance (group
A vs. C, P = 0.07).
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E conversion, mediated by 11ßHSD. Although absolute levels of
urinary THF and 5-THF were similar in all three groups, THE was
significantly elevated in group C (Table 2). Compared with subjects with normal
BMI, this resulted in a significant reduction in the THF+5-THF/THE
ratio (1.06 ± 0.08 to 0.84 ± 0.04; P <
0.05; Fig. 1) and the cortol/cortolone
ratio (0.41 ± 0.03 to 0.34 ± 0.03; P =
0.05) in this group. This change in 11ßHSD activity was not dependent
upon gender, with the mean THF+5-THF/THE ratio falling in men from
1.11 (BMI, <25 kg/m2) to 0.82 (BMI, >30
kg/m2) and in women from 0.99 to 0.85. Overall, the
THF+5-THF/THE ratio was similar in males (0.97 ± 0.07) and
females (0.94 ± 0.04).
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-THF/THE ratio
(t = -3.44; P < 0.01 and
t = 2.39; P < 0.05, respectively),
suggesting that regional fat distribution may be of importance. When
quantified by DEXA scanning, significant relationships were observed
between the THF+5-THF/THE ratio, percent total fat, and regional fat
distribution (Table 3). Inverse
associations were observed between the THF+5-THF/THE ratio and
android fat distribution (scapular and waist), and direct associations
were seen with gynoid fat (hip and thigh) independent of sex. Stepwise
regression indicated that total fat and percent thigh fat were
independent variables in the group as a whole (t =
-2.77; P = 0.009 and t = 2.89;
P = 0.007, respectively). Although regression analysis
indicated a relationship between the percent waist fat and insulin
sensitivity (HOMA -%S; t = -3.46; P
< 0.001), no independent relationship between the THF+5-THF/THE
ratio and insulin/glucose levels (basal or stimulated) and HOMA -%S
was observed.
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-THF ratio was higher in the obese group, and the absolute
levels of THF and 5-THF suggested that this may be due to enhanced
5ß-reductase activity. The etiocholanolone/androsterone ratio was
also higher in the obese group (Table 2
), although these changes did
not reach statistical significance and were not correlated with BMI,
waist/hip ratio, total body fat, or regional fat distribution. A
nonsignificant increase (P = 0.08) in the excretion of
total F metabolites (reflecting the underlying F secretion rate) was
seen in the most severe obese group, but there was no relationship
between total F metabolites and BMI, waist/hip ratio, or regional
adiposity as measured by DEXA analysis.
There was no change in the UFF/UFE ratio between groups, suggesting
similar levels of 11ßHSD2 (23) (Fig. 1). After the oral ingestion of
E acetate, there was a significant reduction in serum F levels in obese
subjects (Fig. 2); taken together, these
data suggest that the changes in the THF+5-THF/THE ratio were indeed
secondary to inhibition of 11ßHSD1.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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E interconversion toward E, indicative of inhibition of the type 1
isozyme of 11ßHSD in patients with obesity. Several studies, some
conducted over 30 yr ago (5, 10), have demonstrated an increased MCR
for cortisol in patients with obesity (9, 11), yet until now the
underlying basis for this has remained unknown. Our demonstration of
inhibition of conversion of E to F would result in an increased net MCR
of F. Circulating F concentrations, however, are normal in obese
subjects, suggesting that this enhanced F metabolism is offset by an
increase in secretion rate. In our study, total F metabolites (known to
accurately reflect the F secretion rate) (28) were increased in obese
subjects, but not significantly so. Other studies have reported
increased F secretion rates in obesity and indicate that this may
reflect enhanced hypothalamic-pituitary-adrenal drive (11). Perhaps the
most florid example of this is seen in patients with the so-called
syndrome of apparent cortisone reductase deficiency. Such patients
present with ACTH-mediated hyperandrogenism and excrete F metabolites
almost exclusively as THE. The presumed genetic defect in 11ßHSD1
results in failure to convert E to F, an increased metabolic rate for
F, and an enhanced F secretion rate at the expense of ACTH-mediated
androgen excess (29, 30). It seems highly likely, therefore, that
obesity reflects a milder, presumably acquired, form of the apparent
cortisone reductase deficiency disorder. A similar picture has been
reported in some studies evaluating women with polycystic ovary
syndrome (31).
Although this is the first study to evaluate F metabolism in this way
in an obese cohort, our data are in keeping with a recent report
analyzing the effect of obesity on F metabolism in patients with
hypopituitarism, where a reduction in the ratio of F/E metabolites was
observed, but in a sex-dependent fashion, in patients with android
obesity (32). These studies conflict with a recent report by Andrew and
colleagues, who claim an increase in the THF/THE ratio in obese males
and reduced THF/5-THF in obesity in both sexes (33). However, that
paper did not examine a controlled obese population per se,
but reported multiple regression analyses from a normal cohort
population. Furthermore, the absolute levels of the urine F metabolites
and their ratios were highly discrepant from published data from our
own and other groups.
The cause of the inhibition of 11ßHSD1 activity remains obscure.
Thyroid hormone is known to regulate 11ßHSD activity (34, 35), but
free thyroid hormone concentrations and TSH were similar in both
groups. Similarly, some studies have shown an inhibitory effect of
insulin on 11ßHSD1 expression (36, 37), although we have been unable
to confirm these findings in our studies on primary cultures of human
adipose stromal cells. Nevertheless, we have meticulously analyzed
insulin sensitivity, and despite demonstrating significant insulin
resistance in our obese subjects, there was no relationship between
insulin levels or sensitivity and the THF+5-THF/THE ratio.
Similarly, the change in 11ßHSD1 activity with obesity was observed
independent of gender, arguing against a major role for sex steroids in
explaining the differences. Striking findings were the correlations
between regional fat distribution and the THF+5-THF/THE ratio;
android obesity (scapular and waist fat) was inversely related, and
gynoid obesity (hip and thigh fat) was directly related to this ratio,
suggesting that EF conversion is reduced in central obesity but
increased in patients with gynoid fat distribution.
At an autocrine level, 11ßHSD1 expression has been shown to facilitate glucocorticoid hormone action in most tissues expressing the enzyme, that is liver (38), gonad (39, 40), central neural tissues (41, 42), and adipose tissue itself. In paired fat biopsy samples, we have recently demonstrated increased expression of 11ßHSD1 in human adipose stromal cells from omental compared with sc depots (21). 11ßHSD1 plays a key role in modulating glucocorticoid-induced adipocyte differentiation (our personal observations, submitted for publication). We have proposed that this differential expression of 11ßHSD1 may explain the discrepant actions of glucocorticoids on different adipose tissue depots and may also be of relevance in the pathogenesis of central obesity. Patients with Cushing’s syndrome develop a reversible form of central obesity, and it is possible that the enhanced conversion of E to F within the omentum itself via 11ßHSD1 expression could result in the same phenotype in non-Cushingoid individuals. The reduction in E to F conversion with increasing central adiposity in this study argues against this hypothesis. The major organ responsible for E to F conversion is probably the liver, and it is possible that the 11ßHSD1 enzyme is regulated differently within liver and adipose tissue. Furthermore, the set-point of F to E conversion may vary at these different sites. In intact hepatocytes, 11ßHSD1 acts exclusively as a reductase (18, 37), and although reductase activity is also present in primary cultures of adipose stromal cells, we have consistently also observed dehydrogenase activity (21). Studies are required to analyze 11ßHSD1 expression and the set-point of F to E conversion in adipose tissue samples from obese and nonobese individuals to clarify whether the reduction in 11ßHSD1 activity observed in our in vivo study is reflected in vitro within adipose tissue. Even so, it has been suggested that inhibition of hepatic 11ßHSD1 activity may improve insulin sensitivity by lowering hepatic glucose output (43). Many of our obese patients demonstrated features of the so-called metabolic syndrome, with central obesity, insulin resistance, and higher lipid levels and blood pressure compared with lean controls, but nevertheless already had reduced hepatic 11ßHSD1 activity. The rationale that further inhibition of 11ßHSD1 activity may be of therapeutic benefit in this group should be reevaluated.
In summary, we have demonstrated striking differences in F metabolism in patients with obesity. The set-point in the interconversion between F and E is shifted toward E, and this occurs because of inhibition of 11ßHSD1 in the setting of unaltered activity of 11ßHSD2. Altered 11ßHSD1 activity cannot be explained by differences in insulin action or thyroid hormone status, but is closely related to body fat distribution, with impaired E to F conversion seen in patients with android or central obesity independent of sex. These data may explain the reported increase in the F MCR seen in obesity, but cast new doubts on the primary role of 11ßHSD1 expression in the pathogenesis of obesity and insulin resistance.
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Acknowledgments |
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Footnotes |
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2 Medical Research Council Senior Clinical Fellow.
Received October 28, 1998.
Revised December 7, 1998.
Accepted December 9, 1998.
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L. M. Watts, V. P. Manchem, T. A. Leedom, A. L. Rivard, R. A. McKay, D. Bao, T. Neroladakis, B. P. Monia, D. M. Bodenmiller, J. X.-C. Cao, et al. Reduction of Hepatic and Adipose Tissue Glucocorticoid Receptor Expression With Antisense Oligonucleotides Improves Hyperglycemia and Hyperlipidemia in Diabetic Rodents Without Causing Systemic Glucocorticoid Antagonism Diabetes, June 1, 2005; 54(6): 1846 - 1853. [Abstract] [Full Text] [PDF]
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R. Andrew, J. Westerbacka, J. Wahren, H. Yki-Jarvinen, and B. R. Walker The Contribution of Visceral Adipose Tissue to Splanchnic Cortisol Production in Healthy Humans Diabetes, May 1, 2005; 54(5): 1364 - 1370. [Abstract] [Full Text] [PDF]
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T. C. Sandeep, R. Andrew, N. Z.M. Homer, R. C. Andrews, K. Smith, and B. R. Walker Increased In Vivo Regeneration of Cortisol in Adipose Tissue in Human Obesity and Effects of the 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Inhibitor Carbenoxolone Diabetes, March 1, 2005; 54(3): 872 - 879. [Abstract] [Full Text] [PDF]
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D. E. Laaksonen, L. Niskanen, K. Punnonen, K. Nyyssonen, T.-P. Tuomainen, V.-P. Valkonen, and J. T. Salonen The Metabolic Syndrome and Smoking in Relation to Hypogonadism in Middle-Aged Men: A Prospective Cohort Study J. Clin. Endocrinol. Metab., February 1, 2005; 90(2): 712 - 719. [Abstract] [Full Text] [PDF]
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M. Korach-Andre, J. Gao, J. S. Gounarides, R. Deacon, A. Islam, and D. Laurent Relationship between visceral adiposity and intramyocellular lipid content in two rat models of insulin resistance Am J Physiol Endocrinol Metab, January 1, 2005; 288(1): E106 - E116. [Abstract] [Full Text] [PDF]
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 J. P. Girod and D. J. Brotman Does altered glucocorticoid homeostasis increase cardiovascular risk? Cardiovasc Res, November 1, 2004; 64(2): 217 - 226. [Abstract] [Full Text] [PDF]
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 J. W. Tomlinson, E. A. Walker, I. J. Bujalska, N. Draper, G. G. Lavery, M. S. Cooper, M. Hewison, and P. M. Stewart 11{beta}-Hydroxysteroid Dehydrogenase Type 1: A Tissue-Specific Regulator of Glucocorticoid Response Endocr. Rev., October 1, 2004; 25(5): 831 - 866. [Abstract] [Full Text] [PDF]
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K. Kannisto, K. H. Pietilainen, E. Ehrenborg, A. Rissanen, J. Kaprio, A. Hamsten, and H. Yki-Jarvinen Overexpression of 11{beta}-Hydroxysteroid Dehydrogenase-1 in Adipose Tissue Is Associated with Acquired Obesity and Features of Insulin Resistance: Studies in Young Adult Monozygotic Twins J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4414 - 4421. [Abstract] [Full Text] [PDF]
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G. Valsamakis, A. Anwar, J. W. Tomlinson, C. H. L. Shackleton, P. G. McTernan, R. Chetty, P. J. Wood, A. K. Banerjee, G. Holder, A. H. Barnett, et al. 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Activity in Lean and Obese Males with Type 2 Diabetes Mellitus J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4755 - 4761. [Abstract] [Full Text] [PDF]
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A. Gambineri, C. Pelusi, E. Manicardi, V. Vicennati, M. Cacciari, A. M. Morselli-Labate, U. Pagotto, and R. Pasquali Glucose Intolerance in a Large Cohort of Mediterranean Women With Polycystic Ovary Syndrome: Phenotype and Associated Factors Diabetes, September 1, 2004; 53(9): 2353 - 2358. [Abstract] [Full Text] [PDF]
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R. Basu, R. J. Singh, A. Basu, E. G. Chittilapilly, C. M. Johnson, G. Toffolo, C. Cobelli, and R. A. Rizza Splanchnic Cortisol Production Occurs in Humans: Evidence for Conversion of Cortisone to Cortisol Via the 11-{beta} Hydroxysteroid Dehydrogenase (11{beta}-HSD) Type 1 Pathway Diabetes, August 1, 2004; 53(8): 2051 - 2059. [Abstract] [Full Text] [PDF]
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J. W. Tomlinson, J. S. Moore, P. M. S. Clark, G. Holder, L. Shakespeare, and P. M. Stewart Weight Loss Increases 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression in Human Adipose Tissue J. Clin. Endocrinol. Metab., June 1, 2004; 89(6): 2711 - 2716. [Abstract] [Full Text] [PDF]
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 J. R. Seckl, N. M. Morton, K. E. Chapman, and B. R. Walker Glucocorticoids and 11beta-Hydroxysteroid Dehydrogenase in Adipose Tissue Recent Prog. Horm. Res., January 1, 2004; 59(1): 359 - 393. [Abstract] [Full Text]
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T. Tsilchorozidou, J. W. Honour, and G. S. Conway Altered Cortisol Metabolism in Polycystic Ovary Syndrome: Insulin Enhances 5{alpha}-Reduction But Not the Elevated Adrenal Steroid Production Rates J. Clin. Endocrinol. Metab., December 1, 2003; 88(12): 5907 - 5913. [Abstract] [Full Text] [PDF]
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J. Westerbacka, H. Yki-Jarvinen, S. Vehkavaara, A.-M. Hakkinen, R. Andrew, D. J. Wake, J. R. Seckl, and B. R. Walker Body Fat Distribution and Cortisol Metabolism in Healthy Men: Enhanced 5{beta}-Reductase and Lower Cortisol/Cortisone Metabolite Ratios in Men with Fatty Liver J. Clin. Endocrinol. Metab., October 1, 2003; 88(10): 4924 - 4931. [Abstract] [Full Text] [PDF]
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M. S. Cooper, A. Blumsohn, P. E. Goddard, W. A. Bartlett, C. H. Shackleton, R. Eastell, M. Hewison, and P. M. Stewart 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Activity Predicts the Effects of Glucocorticoids on Bone J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3874 - 3877. [Abstract] [Full Text] [PDF]
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D. J. Wake, E. Rask, D. E. W. Livingstone, S. Soderberg, T. Olsson, and B. R. Walker Local and Systemic Impact of Transcriptional Up-Regulation of 11{beta}-Hydroxysteroid Dehydrogenase Type 1 in Adipose Tissue in Human Obesity J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3983 - 3988. [Abstract] [Full Text] [PDF]
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C. Mattsson, M. Lai, J. Noble, E. McKinney, J. L. Yau, J. R. Seckl, and B. R. Walker Obese Zucker Rats Have Reduced Mineralocorticoid Receptor and 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression in Hippocampus--Implications for Dysregulation of the Hypothalamic-Pituitary-Adrenal Axis in Obesity Endocrinology, July 1, 2003; 144(7): 2997 - 3003. [Abstract] [Full Text] [PDF]
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R. S. Lindsay, D. J. Wake, S. Nair, J. Bunt, D. E. W. Livingstone, P. A. Permana, P. A. Tataranni, and B. R. Walker Subcutaneous Adipose 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Activity and Messenger Ribonucleic Acid Levels Are Associated with Adiposity and Insulinemia in Pima Indians and Caucasians J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2738 - 2744. [Abstract] [Full Text] [PDF]
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M. N. Kerstens and R. P. F. Dullaart Cortisol Metabolism and Glucose Intolerance J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2951 - 2951. [Full Text] [PDF]
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B. R. Walker and R. Andrew Cortisol Metabolism in Type 2 Diabetes J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2951 - 2952. [Full Text] [PDF]
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Y. Liu, Y. Nakagawa, Y. Wang, R. Li, X. Li, T. Ohzeki, and T. C. Friedman Leptin Activation of Corticosterone Production in Hepatocytes May Contribute to the Reversal of Obesity and Hyperglycemia in Leptin-Deficient ob/ob Mice Diabetes, June 1, 2003; 52(6): 1409 - 1416. [Abstract] [Full Text] [PDF]
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J. W. Tomlinson, N. Crabtree, P. M. S. Clark, G. Holder, A. A. Toogood, C. H. L. Shackleton, and P. M. Stewart Low-Dose Growth Hormone Inhibits 11{beta}-Hydroxysteroid Dehydrogenase Type 1 but Has No Effect upon Fat Mass in Patients with Simple Obesity J. Clin. Endocrinol. Metab., May 1, 2003; 88(5): 2113 - 2118. [Abstract] [Full Text] [PDF]
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 D. E. W. Livingstone and B. R. Walker Is 11beta -Hydroxysteroid Dehydrogenase Type 1 a Therapeutic Target? Effects of Carbenoxolone in Lean and Obese Zucker Rats J. Pharmacol. Exp. Ther., April 1, 2003; 305(1): 167 - 172. [Abstract] [Full Text]
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 T. Dimitriou, C. Maser-Gluth, and T. Remer Adrenocortical activity in healthy children is associated with fat mass Am. J. Clinical Nutrition, March 1, 2003; 77(3): 731 - 736. [Abstract] [Full Text] [PDF]
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R. C. Andrews, O. Rooyackers, and B. R. Walker Effects of the 11{beta}-Hydroxysteroid Dehydrogenase Inhibitor Carbenoxolone on Insulin Sensitivity in Men with Type 2 Diabetes J. Clin. Endocrinol. Metab., January 1, 2003; 88(1): 285 - 291. [Abstract] [Full Text] [PDF]
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D. Tiosano, I. Eisentein, D. Militianu, G. P. Chrousos, and Z.'e. Hochberg 11{beta}-Hydroxysteroid Dehydrogenase Activity in Hypothalamic Obesity J. Clin. Endocrinol. Metab., January 1, 2003; 88(1): 379 - 384. [Abstract] [Full Text] [PDF]
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R. C. Andrews, O. Herlihy, D. E. W. Livingstone, R. Andrew, and B. R. Walker Abnormal Cortisol Metabolism and Tissue Sensitivity to Cortisol in Patients with Glucose Intolerance J. Clin. Endocrinol. Metab., December 1, 2002; 87(12): 5587 - 5593. [Abstract] [Full Text] [PDF]
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J. W. Tomlinson, B. Sinha, I. Bujalska, M. Hewison, and P. M. Stewart Expression of 11{beta}-Hydroxysteroid Dehydrogenase Type 1 in Adipose Tissue Is Not Increased in Human Obesity J. Clin. Endocrinol. Metab., December 1, 2002; 87(12): 5630 - 5635. [Abstract] [Full Text] [PDF]
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S. Diederich, E. Eigendorff, P. Burkhardt, M. Quinkler, C. Bumke-Vogt, M. Rochel, D. Seidelmann, P. Esperling, W. Oelkers, and V. Bahr 11{beta}-Hydroxysteroid Dehydrogenase Types 1 and 2: An Important Pharmacokinetic Determinant for the Activity of Synthetic Mineralo- and Glucocorticoids J. Clin. Endocrinol. Metab., December 1, 2002; 87(12): 5695 - 5701. [Abstract] [Full Text] [PDF]
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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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