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farriery
veterinary
biomechanics
anatomy
nutrition
physiotherapy
2004
Case Report

Tissue-specific dysregulation of cortisol metabolism in equine laminitis.

Authors: Johnson P J, Ganjam V K, Slight S H, Kreeger J M, Messer N T

Journal: Equine veterinary journal

Summary

# Editorial Summary: Tissue-specific dysregulation of cortisol metabolism in equine laminitis Whilst glucocorticoids are suspected contributors to laminitis pathogenesis, the precise mechanisms remain unclear—particularly how local tissue regulation of cortisol activity influences lamellar inflammation and breakdown. Johnson and colleagues investigated whether 11β-hydroxysteroid dehydrogenase-1 (11β-HSD-1), the enzyme responsible for converting inactive cortisone to active cortisol within tissues, showed altered expression in the integumentary structures (hooves and lamellar tissue) during laminitis. Their findings revealed tissue-specific dysregulation of cortisol-metabolising enzymes in affected lamellae, suggesting that localised amplification of glucocorticoid activity within the hoof may exacerbate inflammatory cascades independent of systemic hormone levels. These results have significant implications for understanding endocrinopathic laminitis (particularly in Cushing's disease and PSSM cases) and suggest that future interventions might beneficially target local cortisol metabolism rather than—or in addition to—systemic glucocorticoid suppression. Understanding these tissue-level mechanisms could refine therapeutic approaches and identify biomarkers for laminitis risk in predisposed populations.

Read the full abstract on PubMed

Practical Takeaways

  • Understanding tissue-specific cortisol metabolism could inform new therapeutic targets for laminitis management beyond systemic glucocorticoid modulation
  • Local enzyme activity in lamellar tissue may be a key factor in laminitis susceptibility, suggesting future treatments could focus on tissue-level cortisol regulation rather than whole-body hormonal suppression

Key Findings

  • Local tissue activity of glucocorticoids is regulated by 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) enzyme in skin and hoof lamellar tissue
  • Changes in integumentary 11beta-HSD activity occur during laminitis development
  • Dysregulation of cortisol metabolism in affected tissues may influence glucocorticoid involvement in laminitis pathogenesis

Conditions Studied

laminitis