Cortisol Metabolism in Obesity

Dunkelman, Stanley S.; Fairhurst, B. J.; Plager, John E.; Waterhouse, Christine

doi:10.1210/jcem-24-9-832

Cited by 83 publications

(32 citation statements)

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“…It is well known that cortisol secretion or production is regularly increased in obesity [3,4]. Urinary free cortisol (UFF) and glucocorticoid metabolite excretion rates are frequently elevated in obese subjects [5][6][7].…”

Section: Glucocorticoid Secretion In Obesitymentioning

confidence: 99%

Brief review: Glucocorticoid excretion in obesity

Müssig

Maser-Gluth

2010

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Glucocorticoid Secretion In Obesitymentioning

confidence: 99%

Brief review: Glucocorticoid excretion in obesity

Müssig

Maser-Gluth

2010

The Journal of Steroid Biochemistry and Molecular Biology

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“…Urinary 17-OHCS are influenced by the cortisol secretory rate, rate of cortisol metabolism and renal filtration/excretion. The urinary 17-OHCS are correlated with body mass and thus obese individuals have higher levels than lean individuals (32,38,94,104,113). Urinary 17-OHCS can be adjusted for body mass by dividing by body surface area or urine creatinine.…”

Section: Urinary 17 Hydroxycorticosteroidsmentioning

confidence: 99%

The Hypothalamic‐Pituitary‐Adrenal Axis in Obesity

1995

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“…A BNORMAL METABOLISM OF glucocorticoids has been implicated in the pathophysiology of obesity for many years (1). Glucocorticoids are regulated at the prereceptor level by the microsomal enzyme 11␤-hydroxysteroid dehydrogenase (11␤-HSD), which interconverts active cortisol and inactive cortisone.…”

mentioning

confidence: 99%

Modulation of 11β-Hydroxysteroid Dehydrogenase Type 1 in Mature Human Subcutaneous Adipocytes by Hypothalamic Messengers

Friedberg

Zoumakis

Hiroi

et al. 2003

The Journal of Clinical Endocrinology & Metabolism

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Glucocorticoids are regulated at the prereceptor level by 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), which interconverts inactive cortisone and active cortisol. In a previous study, we noted that patients with hypothalamic obesity had an increased ratio of cortisol/cortisone metabolites, suggesting enhanced 11 beta-HSD-1 activity. In this in vitro study, we tested the hypothesis that adipose 11 beta-HSD-1 is regulated by the hypothalamus via circulating hormones, sympathetic nervous system innervation, and/or cytokines. Preadipocytes were retrieved from sc fat from healthy nonobese individuals and differentiated in vitro to mature adipocytes. Cells were incubated with several potential effectors, and the activity of 11 beta-HSD-1 was assayed by measuring conversion of added 500 nM cortisone to cortisol. Expression of 11 beta-HSD-1 mRNA was determined by real-time PCR, whereas lipolytic effects were determined by measuring glycerol concentration in the culture medium. CRH down-regulated 11 beta-HSD-1 activity with maximal effect at 10(-9)M (65 +/- 10% of control; P < 0.001) and caused a reduction in lipolysis. Likewise, ACTH down-regulated 11 beta-HSD-1 activity with maximal effect at 10(-9) M (65 +/- 20%; P < 0.05) and reduced medium glycerol. Neither CRH nor ACTH affected 11 beta-HSD-1 mRNA expression. TNF alpha up-regulated 11 beta-HSD-1 activity maximally at 0.6 x 10(-9) M (140 +/- 20%; P < 0.001); the same cytokine increased 11 beta-HSD-1 mRNA levels to 3-fold of control (P < 0.05) and increased medium glycerol levels to 165 +/- 14% of control (P < 0.01). IL-1 beta also up-regulated 11 beta-HSD-1 activity maximally at 0.6 x 10(-9) M (160 +/- 33%; P < 0.001) and caused an increase in glycerol levels (159 +/- 11% of control; P < 0.001). Of the adrenergic agonists, salbutamol up-regulated 11 beta-HSD-1 activity maximally at 10(-7) M (162 +/- 46%; P < 0.02), and clonidine down-regulated it at 10(-7) M (82 +/- 15%; P < 0.005). We conclude that possible distinct hypothalamic mediators regulating adipose tissue 11 beta-HSD-1 might include down-regulation of 11 beta-HSD-1 activity by CRH, ACTH, and alpha 2 sympathetic stimulation, and up-regulation of the enzyme by beta 2 sympathetic stimulation and by the cytokines TNFalpha and IL-1 beta.

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Cortisol Metabolism in Obesity

Cited by 83 publications

References 0 publications

Brief review: Glucocorticoid excretion in obesity

Brief review: Glucocorticoid excretion in obesity

The Hypothalamic‐Pituitary‐Adrenal Axis in Obesity

Modulation of 11β-Hydroxysteroid Dehydrogenase Type 1 in Mature Human Subcutaneous Adipocytes by Hypothalamic Messengers

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