Adrenal steroids and the metabolic syndrome

Stephen P. Thomson, Craig S. Stump, L. Romayne Kurukulasuriya, James R. Sowers

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations


The many similarities between the metabolic syndrome and Cushing's syndrome led to the hypothesis that excess glucocorticoids (GC) are part of the pathogenesis linking their features. We review recent work that confirms the initial similarities (obesity, glucose intolerance, hypertension, and hyperlipidemia) and extends them to associated features of both syndromes (osteopenia, hypogonadism, leukocytosis, depression, and muscle weakness). Recent studies report that these features also occur in subclinical Cushing's syndrome, hypercortisolemic depression, and the transgenic overexpression of 11β-hydoxysteroid dehydrogenase type 1 (11β-HSD1) in mouse models of excess GC in adipose tissue. Reducing excess GC - in the clinical syndromes and in the mouse model - reverses many of these features. Because local tissue excess GC may have a central role in the pathogenesis of the metabolic syndrome, selective 11β-HSD1 inhibitors are under active development by several pharmaceutical companies.

Original languageEnglish (US)
Pages (from-to)512-519
Number of pages8
JournalCurrent Hypertension Reports
Issue number6
StatePublished - Dec 1 2007

ASJC Scopus subject areas

  • Internal Medicine


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