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2007
Cohort Study

Dietary fructan carbohydrate increases amine production in the equine large intestine: Implications for pasture-associated laminitis1

Authors: Crawford C., Sepulveda M. F., Elliott J., Harris P. A., Bailey S. R.

Journal: Journal of Animal Science

Summary

# Editorial Summary Pasture-induced laminitis remains a significant clinical problem in equines, with overconsumption of fermentable carbohydrates—particularly fructans abundant in spring and early summer grasses—implicated as a primary trigger, yet the precise biochemical mechanisms remain incompletely understood. Crawford and colleagues investigated whether dietary fructan induces the production of vasoactive amines in the equine large intestine by supplementing normal and laminitis-prone ponies with inulin (3 g/kg bodyweight daily) whilst monitoring faecal and blood chemistry, hindgut pH, and foot temperature over the study period. Inulin supplementation significantly lowered faecal pH from 6.89 to 6.18 and increased faecal tryptamine concentrations 2.5-fold and tyramine 2-fold (P <0.05), though these amines did not appear in circulating plasma at measurable levels, suggesting the intestinal mucosa remained intact despite biochemical perturbation. The absence of differences between laminitis-prone and normal ponies indicates that predisposition to laminitis does not stem from inherent differences in hindgut microflora composition, but rather that pasture-associated laminitis likely results from the magnitude of carbohydrate fermentation overwhelming mucosal defences in susceptible individuals. For practitioners managing at-risk horses, this research reinforces the importance of gradual pasture introduction and careful spring grazing management, as even moderate increases in fermentable carbohydrate can substantially alter the hindgut biochemical environment and potentially trigger clinical disease.

Read the full abstract on PubMed

Practical Takeaways

  • Spring/summer pasture with high fructan content drives hindgut fermentation and amine production—even without clinical signs—in all horses, so gradual pasture introduction and dietary management are critical preventive strategies
  • Laminitis-prone horses do not have fundamentally different hindgut microflora; their predisposition likely involves differential tissue sensitivity to fermentation by-products rather than bacterial overgrowth
  • Monitoring for early laminitis signs during pasture transitions is essential because fecal changes (pH, amines) occur before plasma markers elevate or clinical lameness develops

Key Findings

  • Dietary inulin (fructan) at 3 g/kg body weight reduced fecal pH from 6.89 to 6.18 (P<0.05)
  • Fecal tryptamine increased 2.5-fold and tyramine increased 2-fold with inulin supplementation (P<0.05)
  • No elevation of plasma amines or lactate occurred despite increased fecal amine production, suggesting a threshold for mucosal damage
  • No difference in fecal fermentation products between laminitis-prone and normal ponies, indicating intestinal microflora composition does not explain laminitis predisposition

Conditions Studied

pasture-associated laminitislaminitis predisposition