Physiologic roles of 11β-hydroxysteroid dehydrogenase type 2 in kidney

Isomura, Yukinori; Mune, Tomoatsu; Morita, Hiroyuki; Suwa, Tetsuya; Takada, Nobuki; Yamamoto, Yuhei; Takeda, Jun

doi:10.1016/j.metabol.2006.06.005

Cited by 11 publications

(4 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This and the fact that plasma cortisone falls to values 1/10 of the normal in patients who have undergone bilateral nephrectomy [16] confirms earlier studies that the kidney is the principal source of cortisone in man [110]. Accordingly, measurements of UFF and UFE together in the same urine samples appear to allow a relative specific assessment of renal 11b-HSD2 [16,17,20,[111][112][113].…”

Section: G Role Of Urinary Free Cortisone and 11b-hsd2 In The Non-insupporting

confidence: 74%

Glucocorticoid Measurements in Health and Disease - Metabolic Implications and the Potential of 24-h Urine Analyses

Remer¹,

Maser-Gluth²,

Wudy³

2008

MRMC

View full text Add to dashboard Cite

For examination of glucocorticoid metabolism and identification of hyper and hypocortisolism, various measurements and diagnostic tools are available. After a brief overview of the physiology of glucocorticoid secretion and glucocorticoid actions, the currently used measurements for blood, saliva, and urine samples and the corresponding physiological and metabolic implications are critically reviewed. A special emphasis is placed on the potential of 24-h urine analyses to assess not only glucocorticoid secretion, but also functional glucocorticoid activity.

show abstract

Section: G Role Of Urinary Free Cortisone and 11b-hsd2 In The Non-insupporting

confidence: 74%

Glucocorticoid Measurements in Health and Disease - Metabolic Implications and the Potential of 24-h Urine Analyses

Remer¹,

Maser-Gluth²,

Wudy³

2008

MRMC

View full text Add to dashboard Cite

show abstract

“…The simplified panorama described above must be completed with the influence of agents different from the typical estradiol for estrogen, testosterone for androgen and cortisol (corticosterone in rats) for glucocorticoids. Receptor dimerization and complexity [Sonoda et al, 2008; including their presence in the cell surface (Kim et al, 2008; Levin, 2009) and/or nucleus/cytoplasm (Welshons et al, 1984; Sebastian et al, 2004)], is compounded by the existence of converting enzymes, typically aromatase (Simpson, 2000; Miller, 2006), 17βOH- (Labrie et al, 1997; Adamski and Jakob, 2001) and 11βOH-steroid dehydrogenases (Agarwal, 2003; Isomura et al, 2006). Other hormones, such as progesterone, play a particular role under specific conditions (i.e., pregnancy; Spencer and Bazer, 2002; Gellersen et al, 2009) or act as supplemental signals for the three classical lines described, largely glucocorticoid (and antiglucocorticoid) effects (Pedersen et al, 2003; Zhang et al, 2007).…”

Section: Effects Of Alterations In Steroid Hormone Equilibrium Balancementioning

confidence: 99%

Do the Interactions between Glucocorticoids and Sex Hormones Regulate the Development of the Metabolic Syndrome?

Alemany¹

2012

Front. Endocrin.

View full text Add to dashboard Cite

The metabolic syndrome is basically a maturity-onset disease. Typically, its manifestations begin to flourish years after the initial dietary or environmental aggression began. Since most hormonal, metabolic, or defense responses are practically immediate, the procrastinated response do not seem justified. Only in childhood, the damages of the metabolic syndrome appear with minimal delay. Sex affects the incidence of the metabolic syndrome, but this is more an effect of timing than absolute gender differences, females holding better than males up to menopause, when the differences between sexes tend to disappear. The metabolic syndrome is related to an immune response, countered by a permanent increase in glucocorticoids, which keep the immune system at bay but also induce insulin resistance, alter the lipid metabolism, favor fat deposition, mobilize protein, and decrease androgen synthesis. Androgens limit the operation of glucocorticoids, which is also partly blocked by estrogens, since they decrease inflammation (which enhances glucocorticoid release). These facts suggest that the appearance of the metabolic syndrome symptoms depends on the strength (i.e., levels) of androgens and estrogens. The predominance of glucocorticoids and the full manifestation of the syndrome in men are favored by decreased androgen activity. Low androgens can be found in infancy, maturity, advanced age, or because of their inhibition by glucocorticoids (inflammation, stress, medical treatment). Estrogens decrease inflammation and reduce the glucocorticoid response. Low estrogen (infancy, menopause) again allow the predominance of glucocorticoids and the manifestation of the metabolic syndrome. It is postulated that the equilibrium between sex hormones and glucocorticoids may be a critical element in the timing of the manifestation of metabolic syndrome-related pathologies.

show abstract

“…This enzyme is mainly expressed in the liver and in the adipose tissue, and its expression can be induced in fibroblasts, muscles, and other tissues (934). 11 β -HSD2 converts cortisol to cortisone, and it has been found in tissues that express the mineralocorticoid receptor (especially the kidneys), allowing aldosterone to bind to this receptor [94]. …”

Section: Hypercortisolism and Diabetesmentioning

confidence: 99%

Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology

Dalmazi

Pagotto

Pasquali

et al. 2012

Journal of Nutrition and Metabolism

142

101

View full text Add to dashboard Cite

Type 2 diabetes mellitus is the result of interaction between genetic and environmental factors, leading to heterogeneous and progressive pancreatic β-cell dysfunction. Overweight and obesity are major contributors to the development of insulin resistance and impaired glucose tolerance. The inability of β cells to secrete enough insulin produces type 2 diabetes. Abnormalities in other hormones such as reduced secretion of the incretin glucagon-like peptide 1 (GLP-1), hyperglucagonemia, and raised concentrations of other counterregulatory hormones also contribute to insulin resistance, reduced insulin secretion, and hyperglycaemia in type 2 diabetes. Clinical-overt and experimental cortisol excess is associated with profound metabolic disturbances of intermediate metabolism resulting in abdominal obesity, insulin resistance, and low HDL-cholesterol levels, which can lead to diabetes. It was therefore suggested that subtle abnormalities in cortisol secretion and action are one of the missing links between insulin resistance and other features of the metabolic syndrome. The aim of this paper is to address the role of glucocorticoids on glucose homeostasis and to explain the relationship between hypercortisolism and type 2 diabetes.

show abstract

Physiologic roles of 11β-hydroxysteroid dehydrogenase type 2 in kidney

Cited by 11 publications

References 27 publications

Glucocorticoid Measurements in Health and Disease - Metabolic Implications and the Potential of 24-h Urine Analyses

Glucocorticoid Measurements in Health and Disease - Metabolic Implications and the Potential of 24-h Urine Analyses

Do the Interactions between Glucocorticoids and Sex Hormones Regulate the Development of the Metabolic Syndrome?

Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology

Contact Info

Product

Resources

About