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Endocrinology Unit, Department of Medical Sciences, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, Scotland, United Kingdom
Address all correspondence and requests for reprints to: Professor Jonathan R. Seckl, Endocrinology Unit, Department of Medical Sciences, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, Scotland, United Kingdom. E-mail: J.Seckl{at}ed.ac.uk
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 Top Abstract IntroductionHistoryModulation of Receptor...11ß-HSD1 in Human...Future DirectionsReferences |
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Introduction |
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TopAbstractIntroductionHistoryModulation of Receptor...11ß-HSD1 in Human...Future DirectionsReferences |
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-reductases), oestrogens
(17ß-hydroxysteroid dehydrogenases and aromatase), and thyroid
hormones (5'-monodeiodinases). For glucocorticoids, the key enzymes are
11ß-hydroxysteroid dehydrogenases (11ß-HSDs). Understanding the
tissue-specific functions of 11ß-HSDs has led to new insights into
pathophysiology of common diseases and has suggested novel approaches
to target experimental and therapeutic manipulations of steroid action.
Here we review the emerging biology of 11ß-HSDs with emphasis on the
hitherto rather neglected type 1 isozyme. |
History |
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One or two isozymes of 11ß-HSD?
Monder and colleagues then cloned a complementary DNA (cDNA) using
antibodies raised against their 11ß-HSD purified from rat liver
(9). This cDNA hybridized with a product highly expressed
in rat kidney (10) and was thought to represent the active
11ß-dehydrogenase. However, it became clear that this enzyme could
not explain mineralocorticoid receptor protection in the distal
nephron. For example, it was expressed widely (including in
hippocampus, where mineralocorticoid receptors are not selective for
aldosterone), was of low affinity (micromolar Km
for active 11-hydroxysteroids), and did not match the regulation or
co-factor preference of the 11ß-dehydrogenase activity in distal
nephron. These discrepancies were resolved with the purification
(11) and cloning (12, 13) of a second
isozyme, 11ß-HSD2 (see Fig. 1
).
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Modulation of Receptor Activation by 11ß-HSD1 |
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TopAbstractIntroductionHistoryModulation of Receptor...11ß-HSD1 in Human...Future DirectionsReferences |
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11ß-dehydrogenase or 11ß-reductase?
In original purification studies, the 11ß-HSD1 in the liver was
shown to be bidirectional, although, in contrast with its dehydrogenase
activity, the reductase activity was unstable in vitro
(2). More recently, a series of studies suggest that the
enzyme prefers the reductase direction unless cells are disrupted. This
applies in primary cultures of cells from liver (18),
adipose tissue (19), lung (20), CNS
(21), and vascular smooth muscle (22). In a
few studies, for example in Leydig cells, 11ß-dehydrogenase activity
has been reported in apparently intact cell preparations
(23), but others have found predominant 11ß-reduction
(24) and argued that some 11ß-HSD1 must be liberated
from damaged cells to detect 11ß-dehydrogenase activity. This
striking change in directionality between intact cells and homogenates
has never been satisfactorily explained, but may reflect the specific
intracellular localization of 11ß-HSD1 in the inner leaflet of the
endoplasmic reticulum, where neighboring enzymes may be powerful
generators of the reduced cosubstrate NADPH. Short-term
post-translational changes such as enzyme phosphorylation may also be
pertinent, particularly to the apparent instability of the
11ß-reductase activity in homogenates, but remain to be investigated.
Alternative explanations, such as longer-term posttranslational
modifications (varying N-linked glycosylation) (25) would
not explain why 11ß-HSD1 activity is overwhelmingly reductive in
intact cells and then shows predominant dehydrogenation in homogenates
of these same cells.
These observations in cells suggested a novel role for 11ß-HSD1, involving reactivation rather than inactivation of glucocorticoid. Does this occur in intact organs? Isolated perfused cat (26) or rat (27) liver models suggest that 11ß-HSD1, which is the only isozyme expressed in the liver, is indeed a predominant 11ß-reductase with a high capacity for reactivating 11-ketosteroid substrate over a broad range of substrate concentrations. These findings can be extrapolated to human liver in vivo, since historical work suggests that, on oral administration, cortisone (the first pharmacological glucocorticoid used in man) is rapidly activated to cortisol. Indeed, recent studies confirm that very little oral cortisone reaches the systemic circulation (28) and that hepatic vein cortisol/cortisone ratios are very high (29). 11ß-reductase activity has been shown in other human tissues in vivo, including sc adipose tissue (30).
Availability of substrate
So, 11ß-HSD1 acts as a reductase to reactivate glucocorticoids
in most, if not all, cells in which it is expressed in vivo.
In order for this reactivation to play any physiological role in
regulating receptor exposure (as opposed to a pharmacological role when
cortisone is administered), there would need to be a substantial pool
of substrate inert 11-ketosteroids available. The main source of
11-ketosteroid is 11ß-HSD2, predominantly in kidney
(31). In humans, cortisone circulates at levels around
50–100 nmol/liter, largely unbound to plasma proteins and without a
pronounced diurnal rhythm (29). In contrast, cortisol is
approximately 95% bound, largely to corticosteroid-binding globulin,
giving "free" cortisol levels between approximately 1 nmol/liter at
the diurnal nadir and approximately 100 nmol/liter during the diurnal
peak and on stress. In the rat, plasma concentrations of
11-dehydrocorticosterone are also approximately 50 nmol/liter, though
in the mouse levels are lower around 3–5 nmol/liter (32).
Thus, for at least part of the day, circulating cortisone levels equal
or exceed free cortisol levels and similar ratios pertain in
rodents.
Evidence that 11ß-HSD1 amplifies glucocorticoid action
Early studies had addressed the hypothesis that 11ß-HSD1, like
11ß-HSD2, was a predominant dehydrogenase enzyme, which protected
glucocorticoid receptors, e.g. in testis (33).
However, from the above, it appears that there is an ample supply of
inert substrate that can be reactivated by predominant 11ß-reductase
activity of 11ß-HSD1 in many tissues in vivo. What is the
evidence that this influences local glucocorticoid receptor
activation?
Liver. The most persuasive data that 11ß-HSD1 increases effective intracellular glucocorticoid action have been obtained in liver. Here, glucocorticoids oppose the actions of insulin, for example, by up-regulating expression of the rate-limiting enzyme for gluconeogenesis, phosphoenol-pyruvate carboxykinase (PEPCK). In male rats, estradiol potently down regulates 11ß-HSD1 expression (34) and, only in the presence of glucocorticoids, also down-regulates PEPCK expression (35). Such indirect studies, as well as the use of relatively nonselective liquorice-based inhibitors, indicate that impaired activity of 11ß-HSD1 in liver is associated with features of reduced glucocorticoid action and increased insulin sensitivity in hepatocytes.
To explore this further, 11ß-HSD1 knock-out mice have been generated (32). These mice appear to develop normally and are viable, fertile, and normotensive. This model shows that 11ß-HSD1 is the sole major 11ß-reductase, at least in mice, since adrenalectomized knockout mice cannot convert administered 11-dehydrocorticosterone to active corticosterone. However, despite slightly elevated basal plasma corticosterone levels (see below), 11ß-HSD1 -/- mice have a phenotype compatible with impaired intracellular glucocorticoid regeneration and reduced antagonism of insulin action. For example, they show impaired induction of PEPCK and glucose-6-phosphatase on fasting and a lesser hyperglycemic response to stress or induction of obesity (32).
These findings are supported by experiments in healthy humans using the liquorice derivative carbenoxolone to inhibit 11ß-HSD1 activity (36). This is similarly associated with enhanced insulin sensitivity, as measured in a euglycaemic hyperinsulinaemic clamp study, although it remains to be demonstrated whether this is due to altered glucose dynamics in liver and/or peripheral tissues such as adipose.
Brain. There is also good evidence that 11ß-reductase modulates glucocorticoid action in brain. In the CNS, glucocorticoids regulate key developmental, metabolic, neurotransmitter and structural functions, particularly in neurons. Chronic glucocorticoid excess has deleterious effects most notably in the hippocampus, which has a very high density of receptors. 11ß-HSD1 is highly expressed in hippocampus as well as other CNS regions (37). As elsewhere, 11ß-HSD1 in hippocampal cells is a reductase, amplifying glucocorticoid action. Indeed, 11-dehydrocorticosterone is as potent as corticosterone in potentiating excitatory amino acid neurotoxicity in vitro, an effect lost on inhibition of the enzyme (21). Use of liquorice-based inhibitors has not supported the notion that this reaction is important in hippocampal function/neuronal survival in vivo (38). However, such compounds penetrate the CNS rather patchily (39) and are relatively nonselective [i.e. inhibit both 11ß-HSD isozymes, as well as other enzymes of steroid metabolism and even prostaglandin degradation (40)]. Preliminary studies in 11ß-HSD1 null mice support the notion that the enzyme attenuates the deleterious effects of chronic glucocorticoid excess upon cognitive function (Yau et al., 40A ).
Expression of 11ß-HSD1 in hippocampus, hypothalamus, and pituitary also suggests that it may influence negative feedback regulation of the hypothalamic-pituitary-adrenal axis (HPA) by endogenous glucocorticoids. 11ß-HSD1 null mice have adrenocortical hypertrophy and increased responses of the adrenal to ACTH in vitro (32). This could be explained because they are unable to regenerate glucocorticoids in the periphery and hence have enhanced metabolic clearance rate. However, plasma levels of corticosterone are also modestly elevated at the diurnal nadir, findings suggestive of HPA axis activation over and above that required to compensate for altered peripheral clearance. Such effects might be due to either increased forward drive to the HPA axis and/or to attenuated glucocorticoid feedback control. Recent data suggest that this is, at least in part, due to blunted sensitivity to glucocorticoid feedback, since administration of a dose of cortisol that suppresses the HPA responses to a subsequent stressor in wild-type mice fails to do so in 11ß-HSD1 null mice (41).
Other glucocorticoid targets. In some tissues, the role of 11ß-HSD1 has been more difficult to establish because of nearby expression of 11ß-HSD2. An example is in the blood vessel wall. Here, glucocorticoids and mineralocorticoids act on many targets to influence vascular responses. Early data showed expression of 11ß-HSD1 in vascular smooth muscle (42) with potentiation of responses to glucocorticoids by liquorice derivatives (43), suggesting predominant 11ß-dehydrogenase activity. However, 11ß-HSD2 has recently been described in endothelial cells (44) where glucocorticoids influence nitric oxide generation (45). 11ß-HSD1 knockout mice have normal vascular function, whereas 11ß-HSD2 knockout mice have endothelial dysfunction. Whether reactivation of glucocorticoids by 11ß-HSD1 in vascular smooth muscle offsets the influence of 11ß-HSD2 in the endothelium remains to be established.
In many other tissues, descriptive studies suggest an association between 11ß-HSD1 expression and the necessity for adequate exposure to glucocorticoids. These are not reviewed in detail here (see Refs. 16, 17) but include ovarian granulosa cells, cells within the eye, stromal cells in the lymph node, and the lung.
Role of 11ß-HSD1 in the coordinated control of metabolic
function
Having established that 11ß-HSD1 can modulate glucocorticoid
action in key sites controlling metabolic fuel utilization, the next
step will be to understand how these effects are regulated and
integrated in the metabolic responses to environmental stimuli. In
contrast with 11ß-HSD2, which provides a constitutive barrier against
glucocorticoid access to receptors, 11ß-HSD1 expression is highly
regulated. Factors influencing 11ß-HSD1 expression and activity
include glucocorticoids, thyroid hormones, sex steroids, GH, IGF-1,
insulin, and cytokines. These are not reviewed in detail here (see
Refs. 16, 17). A clear synthesis of the physiological
importance of these factors remains elusive, in part because studies of
these processes have been hampered by variations between species and
between tissues. However, several recent strands suggest that
11ß-HSD1 has a place in coordinated metabolic control. For example,
in the long term, chronic stress or elevated glucocorticoid levels
appear to attenuate 11ß-HSD activity (46), at least in
liver and hippocampus. This might represent a homeostatic mechanism to
reduce excessive metabolic effects of glucocorticoids during chronic
stress, while maintaining exposure of other peripheral tissues
(e.g. in the immune system) to elevated circulating
glucocorticoid levels.
Very recent studies have attempted to elucidate the molecular basis for
regulation of 11ß-HSD1. In the rat, the promoter is predominantly
regulated, at least in liver, by the C/EBP family of transcription
factors (47), mainly C/EBP. C/EBP coordinately
regulates a series of genes concerned with the metabolism of fuels and
is in turn regulated by glucocorticoids. It has been suggested that
such cross-talk allows C/EBP to regulate not only its direct target
genes but also to amplify glucocorticoid action, engendering a
coordinate response to metabolic challenge (47). Similar
pathway cross-talk may occur with other transcription factors. Thus,
PPAR ligands, such as fibrates, attenuate 11ß-HSD1
(48). This action may allow PPAR activators to reduce
triglyceride levels both directly via PPAR target genes and
indirectly via reduced 11ß-HSD1 amplification of glucocorticoid
target gene expression in liver. Such speculations remain to be
directly analyzed. The basis of the tissue-specific responses of
11ß-HSD1 to transcriptional and other regulation also remains a key
target for determination.
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11ß-HSD1 in Human Disease |
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TopAbstractIntroductionHistoryModulation of Receptor...11ß-HSD1 in Human...Future DirectionsReferences |
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A handful of patients with apparent congenital cortisone reductase deficiency have been described, but none has had mutations in the coding regions of the 11ß-HSD1 gene (28, 51). This suggests that either another enzyme is responsible for the apparent loss of 11ß-reductase or, more likely, that the deficit lies at the level of gene regulation. Mutations in promoter or intronic regions have not as yet been fully screened. Whatever the etiology, such patients show the predicted exaggerated HPA axis function with increased adrenal androgen production. Measurements of glucocorticoid responses in target tissues such as liver and fat have not been made.
Impaired 11ß-HSD1 may also be important in more common clinical syndromes. In the leptin-resistant Zucker obese rat, 11ß-HSD1 is impaired in liver, a change predicted to ameliorate the local intrahepatic metabolic consequences of the obesity (52). However, this may also activate the HPA axis to compensate for the increased clearance of glucocorticoids though reduced hepatic regeneration. It appears that similarly impaired hepatic 11ß-HSD1 in liver occurs in patients with polycystic ovary syndrome (53) and primary obesity (54, 55).
An alternative possibility is that enhanced 11ß-HSD1 is important in increasing local glucocorticoid action and promoting adverse metabolic effects. In the face of impaired 11ß-HSD1 activity in liver, Zucker obese rats show selectively enhanced activity of 11ß-HSD1 in omental adipose tissue (52). Very recent studies suggest the same tissue-specific pattern of dysregulation of 11ß-HSD1 (i.e. impaired in liver, enhanced in adipose tissue) in human obesity (30, 55).
Finally, whether or not altered 11ß-HSD1 is involved in the pathophysiology of a disorder, manipulation of enzyme activity may provide a means of manipulating glucocorticoid action in specific tissues without affecting circulating cortisol levels. For example, studies in rats show that 11ß-HSD1 is down-regulated, at least in liver, by continuous (female pattern) GH administration (34). Administration of daily GH to hypopituitary patients also results in lower ratios of cortisol/cortisone metabolites consistent with inhibition of 11ß-HSD1 (56). It is intriguing to think that a resultant lowering of intraadipose cortisol concentrations contributes to the reduction in body fat that accompanies GH therapy in these patients. Similarly, the observation that an inhibitor of 11ß-HSD1, carbenoxolone, enhances insulin sensitivity in healthy volunteers (36) offers the tantalizing prospect that selective 11ß-HSD1 inhibitors will be novel insulin-sensitizing agents.
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Future Directions |
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TopAbstractIntroductionHistoryModulation of Receptor...11ß-HSD1 in Human...Future DirectionsReferences |
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It will be important to determine what are the major controls of enzyme reaction direction in vivo since swinging the balance between reduction and dehydrogenation might be an alternative approach to manipulating tissue glucocorticoid levels. A key step will be to obtain a crystallographic structure for the enzyme and understand its interactions with substrates and cofactors. It is also crucial to work out the molecular basis for tissue-specific regulation of 11ß-HSD1. The potential to manipulate this enzyme in a tissue-specific manner opens up intriguing investigational and therapeutic possibilities. The role of 11ß-HSD1, notably at the tissue-specific level, requires to be dissected in humans. Current measures of overall enzyme activity using GC-MS estimations of urinary metabolites are blunt, and removing cells into culture is anticipated per se to alter enzyme expression and potentially kinetics. Finally, studies of 11ß-HSD1 gene structure, polymorphisms and haplotypes will perhaps help explain heterogeneity of activity and regulation in the population.
This review illustrates how fundamental observations during the last 5 yr have been applied rapidly in physiological and pharmacological studies of 11ß-HSD1. The next 5 yr will likely reveal just how complex and valuable the 11ß-HSD system may be.
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Footnotes |
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Received November 20, 2000.
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References |
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TopAbstractIntroductionHistoryModulation of Receptor...11ß-HSD1 in Human...Future DirectionsReferences |
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- and
3ß-hydroxysteroid dehydrogenases and 5- and 5ß-reductase
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regulates hepatic
transcription of 11ß-hydroxysteroid dehydrogenase type 1: a novel
mechanism for cross-talk between the C/EBP and glucocorticoid
signalling pathways. J Biol Chem 275:30232–30239 agonists reduce the expression of 11ßHSD1 in the liver.
Biochem Biophys Res Commun 279:330–336[CrossRef][Medline]
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K. C. Jonas, C. Chandras, D. R. E. Abayasekara, and A. E. Michael Role for Prostaglandins in the Regulation of Type 1 11{beta}-Hydroxysteroid Dehydrogenase in Human Granulosa-Lutein Cells Endocrinology, December 1, 2006; 147(12): 5865 - 5872. [Abstract] [Full Text] [PDF]
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S. A. Reini, C. E. Wood, E. Jensen, and M. Keller-Wood Increased maternal cortisol in late-gestation ewes decreases fetal cardiac expression of 11beta-HSD2 mRNA and the ratio of AT1 to AT2 receptor mRNA Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2006; 291(6): R1708 - R1716. [Abstract] [Full Text] [PDF]
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K Vagnerova, M Kverka, P Klusonova, P Ergang, I Miksik, H Tlaskalova-Hogenova, and J Pacha Intestinal inflammation modulates expression of 11{beta}-hydroxysteroid dehydrogenase in murine gut. J. Endocrinol., November 1, 2006; 191(2): 497 - 503. [Abstract] [Full Text] [PDF]
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 C. M. Pariante The glucocorticoid receptor: part of the solution or part of the problem? J Psychopharmacol, July 1, 2006; 20(4_suppl): 79 - 84. [Abstract] [PDF]
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J. S. Gilmour, A. E. Coutinho, J.-F. Cailhier, T. Y. Man, M. Clay, G. Thomas, H. J. Harris, J. J. Mullins, J. R. Seckl, J. S. Savill, et al. Local amplification of glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1 promotes macrophage phagocytosis of apoptotic leukocytes. J. Immunol., June 15, 2006; 176(12): 7605 - 7611. [Abstract] [Full Text] [PDF]
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A. Gambineri, V. Vicennati, S. Genghini, F. Tomassoni, U. Pagotto, R. Pasquali, and B. R. Walker Genetic Variation in 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Predicts Adrenal Hyperandrogenism among Lean Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2295 - 2302. [Abstract] [Full Text] [PDF]
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W. Li, L. Gao, Y. Wang, T. Duan, L. Myatt, and K. Sun Enhancement of Cortisol-Induced 11{beta}-Hydroxysteroid dehydrogenase Type 1 Expression by Interleukin 1{beta} in Cultured Human Chorionic Trophoblast Cells Endocrinology, May 1, 2006; 147(5): 2490 - 2495. [Abstract] [Full Text] [PDF]
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J. A. Shoener, R. Baig, and K. C. Page Prenatal exposure to dexamethasone alters hippocampal drive on hypothalamic-pituitary-adrenal axis activity in adult male rats Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2006; 290(5): R1366 - R1373. [Abstract] [Full Text] [PDF]
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S. K. Paulsen, S. B. Pedersen, J. O. L. Jorgensen, S. Fisker, J. S. Christiansen, A. Flyvbjerg, and B. Richelsen Growth Hormone (GH) Substitution in GH-Deficient Patients Inhibits 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Messenger Ribonucleic Acid Expression in Adipose Tissue J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 1093 - 1098. [Abstract] [Full Text] [PDF]
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 M. Keller-Wood, M. J. Powers, J. A. Gersting, N. Ali, and C. E. Wood Genomic analysis of neuroendocrine development of fetal brain-pituitary-adrenal axis in late gestation Physiol Genomics, February 23, 2006; 24(3): 218 - 224. [Abstract] [Full Text] [PDF]
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K. L. McCormick, X. Wang, and G. J. Mick Evidence That the 11 {beta}-Hydroxysteroid Dehydrogenase (11 {beta}-HSD1) Is Regulated by Pentose Pathway Flux: STUDIES IN RAT ADIPOCYTES AND MICROSOMES J. Biol. Chem., January 6, 2006; 281(1): 341 - 347. [Abstract] [Full Text] [PDF]
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 M. B. Zemel The Role of Dairy Foods in Weight Management J. Am. Coll. Nutr., December 1, 2005; 24(suppl_6): 537S - 546S. [Abstract] [Full Text] [PDF]
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M. Baserga, M. A. Hale, R. A. McKnight, X. Yu, C. W. Callaway, and R. H. Lane Uteroplacental insufficiency alters hepatic expression, phosphorylation, and activity of the glucocorticoid receptor in fetal IUGR rats Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2005; 289(5): R1348 - R1353. [Abstract] [Full Text] [PDF]
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 L. Freeman, M. Hewison, S. V. Hughes, K. N. Evans, D. Hardie, T. K. Means, and R. Chakraverty Expression of 11{beta}-hydroxysteroid dehydrogenase type 1 permits regulation of glucocorticoid bioavailability by human dendritic cells Blood, September 15, 2005; 106(6): 2042 - 2049. [Abstract] [Full Text] [PDF]
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 R. S. Weinstein 11{beta}-HSD: Guardian or Gate Crasher? IBMS BoneKEy, September 1, 2005; 2(9): 6 - 13. [Full Text] [PDF]
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J. M. Paterson, J. R. Seckl, and J. J. Mullins Genetic manipulation of 11{beta}-hydroxysteroid dehydrogenases in mice Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2005; 289(3): R642 - R652. [Abstract] [Full Text] [PDF]
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 G. R. Small, P. W. F. Hadoke, I. Sharif, A. R. Dover, D. Armour, C. J. Kenyon, G. A. Gray, and B. R. Walker Preventing local regeneration of glucocorticoids by 11{beta}-hydroxysteroid dehydrogenase type 1 enhances angiogenesis PNAS, August 23, 2005; 102(34): 12165 - 12170. [Abstract] [Full Text] [PDF]
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R.-S. Ge, Q. Dong, E.-m. Niu, C. M. Sottas, D. O. Hardy, J. F. Catterall, S. A. Latif, D. J. Morris, and M. P. Hardy 11{beta}-Hydroxysteroid Dehydrogenase 2 in Rat Leydig Cells: Its Role in Blunting Glucocorticoid Action at Physiological Levels of Substrate Endocrinology, June 1, 2005; 146(6): 2657 - 2664. [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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 M. Eijken, M. Hewison, M. S. Cooper, F. H. de Jong, H. Chiba, P. M. Stewart, A. G. Uitterlinden, H. A. P. Pols, and J. P. T. M. van Leeuwen 11{beta}-Hydroxysteroid Dehydrogenase Expression and Glucocorticoid Synthesis Are Directed by a Molecular Switch during Osteoblast Differentiation Mol. Endocrinol., March 1, 2005; 19(3): 621 - 631. [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. J. Hosfield, Y. Wu, R. J. Skene, M. Hilgers, A. Jennings, G. P. Snell, and K. Aertgeerts Conformational Flexibility in Crystal Structures of Human 11{beta}-Hydroxysteroid Dehydrogenase Type I Provide Insights into Glucocorticoid Interconversion and Enzyme Regulation J. Biol. Chem., February 11, 2005; 280(6): 4639 - 4648. [Abstract] [Full Text] [PDF]
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D. Ogg, B. Elleby, C. Norstrom, K. Stefansson, L. Abrahmsen, U. Oppermann, and S. Svensson The Crystal Structure of Guinea Pig 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Provides a Model for Enzyme-Lipid Bilayer Interactions J. Biol. Chem., February 4, 2005; 280(5): 3789 - 3794. [Abstract] [Full Text] [PDF]
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A. J. Drake, D. E. W. Livingstone, R. Andrew, J. R. Seckl, N. M. Morton, and B. R. Walker Reduced Adipose Glucocorticoid Reactivation and Increased Hepatic Glucocorticoid Clearance as an Early Adaptation to High-Fat Feeding in Wistar Rats Endocrinology, February 1, 2005; 146(2): 913 - 919. [Abstract] [Full Text] [PDF]
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T. Y. Zhang, X. Ding, and R. A. Daynes The Expression of 11{beta}-Hydroxysteroid Dehydrogenase Type I by Lymphocytes Provides a Novel Means for Intracrine Regulation of Glucocorticoid Activities J. Immunol., January 15, 2005; 174(2): 879 - 889. [Abstract] [Full Text] [PDF]
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Y. Liu, Y. Nakagawa, Y. Wang, R. Sakurai, P. V. Tripathi, K. Lutfy, and T. C. Friedman Increased Glucocorticoid Receptor and 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression in Hepatocytes May Contribute to the Phenotype of Type 2 Diabetes in db/db Mice Diabetes, January 1, 2005; 54(1): 32 - 40. [Abstract] [Full Text] [PDF]
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 H. Jahn, M. Schick, F. Kiefer, M. Kellner, A. Yassouridis, and K. Wiedemann Metyrapone as Additive Treatment in Major Depression: A Double-blind and Placebo-Controlled Trial Arch Gen Psychiatry, December 1, 2004; 61(12): 1235 - 1244. [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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M. Berthiaume, H. Sell, J. Lalonde, Y. Gelinas, A. Tchernof, D. Richard, and Y. Deshaies Actions of PPAR{gamma} agonism on adipose tissue remodeling, insulin sensitivity, and lipemia in absence of glucocorticoids Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2004; 287(5): R1116 - R1123. [Abstract] [Full Text] [PDF]
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 P. W. Franks, W. C. Knowler, S. Nair, J. Koska, Y.-H. Lee, R. S. Lindsay, B. R. Walker, H. C. Looker, P. A. Permana, P. A. Tataranni, et al. Interaction Between an 11{beta}HSD1 Gene Variant and Birth Era Modifies the Risk of Hypertension in Pima Indians Hypertension, November 1, 2004; 44(5): 681 - 688. [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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G. Banhegyi, A. Benedetti, R. Fulceri, and S. Senesi Cooperativity between 11{beta}-Hydroxysteroid Dehydrogenase Type 1 and Hexose-6-phosphate Dehydrogenase in the Lumen of the Endoplasmic Reticulum J. Biol. Chem., June 25, 2004; 279(26): 27017 - 27021. [Abstract] [Full Text] [PDF]
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E. E. Kershaw and J. S. Flier Adipose Tissue as an Endocrine Organ J. Clin. Endocrinol. Metab., June 1, 2004; 89(6): 2548 - 2556. [Abstract] [Full Text] [PDF]
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K. J. McInnes, C. J. Kenyon, K. E. Chapman, D. E. W. Livingstone, L. J. Macdonald, B. R. Walker, and R. Andrew 5{alpha}-Reduced Glucocorticoids, Novel Endogenous Activators of the Glucocorticoid Receptor J. Biol. Chem., May 28, 2004; 279(22): 22908 - 22912. [Abstract] [Full Text] [PDF]
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J. M. Paterson, N. M. Morton, C. Fievet, C. J. Kenyon, M. C. Holmes, B. Staels, J. R. Seckl, and J. J. Mullins Metabolic syndrome without obesity: Hepatic overexpression of 11{beta}-hydroxysteroid dehydrogenase type 1 in transgenic mice PNAS, May 4, 2004; 101(18): 7088 - 7093. [Abstract] [Full Text] [PDF]
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T. C. Sandeep, J. L. W. Yau, A. M. J. MacLullich, J. Noble, I. J. Deary, B. R. Walker, and J. R. Seckl From The Cover: 11{beta}-Hydroxysteroid dehydrogenase inhibition improves cognitive function in healthy elderly men and type 2 diabetics PNAS, April 27, 2004; 101(17): 6734 - 6739. [Abstract] [Full Text] [PDF]
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M. Duclos, C. Gouarne, C. Martin, C. Rocher, P. Mormede, and T. Letellier Effects of corticosterone on muscle mitochondria identifying different sensitivity to glucocorticoids in Lewis and Fischer rats Am J Physiol Endocrinol Metab, February 1, 2004; 286(2): E159 - E167. [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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K. Sun and L. Myatt Enhancement of Glucocorticoid-Induced 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression by Proinflammatory Cytokines in Cultured Human Amnion Fibroblasts Endocrinology, December 1, 2003; 144(12): 5568 - 5577. [Abstract] [Full Text] [PDF]
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H.G. Klemcke, R. Sampath Kumar, K. Yang, J.L. Vallet, and R.K. Christenson 11{beta}-Hydroxysteroid Dehydrogenase and Glucocorticoid Receptor Messenger RNA Expression in Porcine Placentae: Effects of Stage of Gestation, Breed, and Uterine Environment Biol Reprod, December 1, 2003; 69(6): 1945 - 1950. [Abstract] [Full Text] [PDF]
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C. Christy, P. W.F. Hadoke, J. M. Paterson, J. J. Mullins, J. R. Seckl, and B. R. Walker 11{beta}-Hydroxysteroid Dehydrogenase Type 2 in Mouse Aorta: Localization and Influence on Response to Glucocorticoids Hypertension, October 1, 2003; 42(4): 580 - 587. [Abstract] [Full Text] [PDF]
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 C. L. Raison and A. H. Miller When Not Enough Is Too Much: The Role of Insufficient Glucocorticoid Signaling in the Pathophysiology of Stress-Related Disorders Am J Psychiatry, September 1, 2003; 160(9): 1554 - 1565. [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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 L.M. Thurston, D.P. Norgate, K.C. Jonas, L. Gregory, P.J. Wood, B.A. Cooke, and A.E. Michael Ovarian modulators of type 1 11{beta}-hydroxysteroid dehydrogenase (11{beta}HSD) activity and intra-follicular cortisol:cortisone ratios correlate with the clinical outcome of IVF Hum. Reprod., August 1, 2003; 18(8): 1603 - 1612. [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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B. J. Waddell, S. Hisheh, Z. S. Krozowski, and P. J. Burton Localization of 11{beta}-Hydroxysteroid Dehydrogenase Types 1 and 2 in the Male Reproductive Tract Endocrinology, July 1, 2003; 144(7): 3101 - 3106. [Abstract] [Full Text] [PDF]
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 H. Raff and J. W. Findling A Physiologic Approach to Diagnosis of the Cushing Syndrome Ann Intern Med, June 17, 2003; 138(12): 980 - 991. [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. Kusakabe, I. Nakamura, and G. Young 11{beta}-Hydroxysteroid Dehydrogenase Complementary Deoxyribonucleic Acid in Rainbow Trout: Cloning, Sites of Expression, and Seasonal Changes in Gonads Endocrinology, June 1, 2003; 144(6): 2534 - 2545. [Abstract] [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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 S. Suzuki, K. Koyama, A. Darnel, H. Ishibashi, S. Kobayashi, H. Kubo, T. Suzuki, H. Sasano, and Z. S. Krozowski Dexamethasone Upregulates 11{beta}-Hydroxysteroid Dehydrogenase Type 2 in BEAS-2B Cells Am. J. Respir. Crit. Care Med., May 1, 2003; 167(9): 1244 - 1249. [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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M. Liang, B. Yuan, E. Rute, A. S. Greene, M. Olivier, and A. W. Cowley Jr. Insights into Dahl salt-sensitive hypertension revealed by temporal patterns of renal medullary gene expression Physiol Genomics, February 6, 2003; 12(3): 229 - 237. [Abstract] [Full Text] [PDF]
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N. Shafqat, B. Elleby, S. Svensson, J. Shafqat, H. Jornvall, L. Abrahmsen, and U. Oppermann Comparative Enzymology of 11beta -Hydroxysteroid Dehydrogenase Type 1 from Glucocorticoid Resistant (Guinea Pig) Versus Sensitive (Human) Species J. Biol. Chem., January 10, 2003; 278(3): 2030 - 2035. [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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E. Kajantie, L. Dunkel, U. Turpeinen, U.-H. Stenman, P. J. Wood, M. Nuutila, and S. Andersson Placental 11{beta}-Hydroxysteroid Dehydrogenase-2 and Fetal Cortisol/Cortisone Shuttle in Small Preterm Infants J. Clin. Endocrinol. Metab., January 1, 2003; 88(1): 493 - 500. [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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K. Sun, P. He, and K. Yang Intracrine Induction of 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression by Glucocorticoid Potentiates Prostaglandin Production in the Human Chorionic Trophoblast Biol Reprod, November 1, 2002; 67(5): 1450 - 1455. [Abstract] [Full Text] [PDF]
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T. M. Stulnig, U. Oppermann, K. R. Steffensen, G. U. Schuster, and J.-A. Gustafsson Liver X Receptors Downregulate 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression and Activity Diabetes, August 1, 2002; 51(8): 2426 - 2433. [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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O. Paulmyer-Lacroix, S. Boullu, C. Oliver, M.-C. Alessi, and M. Grino Expression of the mRNA Coding for 11{beta}-Hydroxysteroid Dehydrogenase Type 1 in Adipose Tissue from Obese Patients: An in Situ Hybridization Study J. Clin. Endocrinol. Metab., June 1, 2002; 87(6): 2701 - 2705. [Abstract] [Full Text] [PDF]
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 R. E. Booth, J. P. Johnson, and J. D. Stockand ALDOSTERONE Advan Physiol Educ, March 1, 2002; 26(1): 8 - 20. [Abstract] [Full Text] [PDF]
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G.-M. Wang, R.-S. Ge, S. A. Latif, D. J. Morris, and M. P. Hardy Expression of 11{beta}-Hydroxylase in Rat Leydig Cells Endocrinology, February 1, 2002; 143(2): 621 - 626. [Abstract] [Full Text] [PDF]
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 H. Masuzaki, J. Paterson, H. Shinyama, N. M. Morton, J. J. Mullins, J. R. Seckl, and J. S. Flier A Transgenic Model of Visceral Obesity and the Metabolic Syndrome Science, December 7, 2001; 294(5549): 2166 - 2170. [Abstract] [Full Text] [PDF]
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 P. W.F. Hadoke, C. Christy, Y. V. Kotelevtsev, B. C. Williams, C. J. Kenyon, J. R. Seckl, J. J. Mullins, and B. R. Walker Endothelial Cell Dysfunction in Mice After Transgenic Knockout of Type 2, but Not Type 1, 11{beta}-Hydroxysteroid Dehydrogenase Circulation, December 4, 2001; 104(23): 2832 - 2837. [Abstract] [Full Text] [PDF]
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