Research

Hormonal

In obese women, increased adipose tissue 11β-HSD1 activity regenerates cortisol locally, contributing to central obesity and insulin resistance, while impaired hepatic conversion of cortisone to cortisol leads to compensatory HPA axis activation without raising circulating cortisol levels.

For obese women, high body fat is linked to increased activity of an enzyme (11β-HSD1) in fat tissue that converts inactive cortisone into active cortisol locally. This local excess drives insulin resistance and fat accumulation, even if blood cortisol levels appear normal. Future treatments may target this specific enzyme in fat rather than just managing stress or blood cortisol levels.

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In obese females increased reactivation of glucocorticoids in fat may contribute to the characteristics of the metabolic syndrome. Increased inactivation of cortisol in liver may be responsible for compensatory activation of the HPA axis.
Eva Rask et al. · The Journal of Clinical Endocrinology & Metabolism · 2002

Why this rating

Observational study with strong mechanistic data (biopsies, pharmacokinetics) in a specific population (obese women), but lacks interventional proof of causality in humans.

Source

Tissue-Specific Changes in Peripheral Cortisol Metabolism in Obese Women: Increased Adipose 11β-Hydroxysteroid Dehydrogenase Type 1 Activity

Eva Rask et al. · The Journal of Clinical Endocrinology & Metabolism · 2002

DOI 10.1210/jcem.87.7.8661

cross_sectional · n=41Cited 383×
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DOI resolved against Crossref · corpus check 2026-06-10

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