Executive Summary
Hyperinsulinemia in horses is now widely recognized as a primary driver of endocrinopathic laminitis, the most common form of metabolic laminitis associated with insulin dysregulation in horses and equine metabolic syndrome (EMS). Unlike inflammatory equine laminitis secondary to systemic illness, hormone-driven laminitis develops when sustained elevations in insulin alter lamellar epithelial cell function (Durham et al., 2019; Grenager, 2021).
Introduction
A healthy-looking horse suddenly develops equine laminitis with no obvious trauma, infection, or systemic illness. Digital pulses become bounding, the stance changes subtly, and discomfort appears without warning. Increasingly, such cases are traced to hyperinsulinemia in horses rather than inflammatory disease.
What Is Hyperinsulinemia?
Hyperinsulinemia in horses refers to elevated circulating insulin concentrations beyond normal physiological ranges. It may present as resting hyperinsulinemia or as exaggerated post-prandial hyperinsulinemia following dietary carbohydrate exposure.
The Insulin–Lamellar Connection
The lamellae suspend the distal phalanx inside the hoof capsule through an intricate dermal–epidermal interface. These lamellar epithelial cells are metabolically active and hormonally responsive.
Research confirms that IGF-1 receptors are present in lamellar tissue and that high insulin concentrations can activate these cells through the IGF-1 receptor laminitis pathway (Baskerville et al., 2018). Complementary studies in endocrinopathic laminitis models demonstrate lamellar events consistent with IGF-1 receptor signaling involvement (Lane et al., 2017).
The IGF-1 Receptor Pathway
The IGF-1 receptor laminitis pathway provides a molecular explanation for hormone-driven laminitis. When insulin concentrations exceed physiological norms, insulin may cross-activate IGF-1 receptors in lamellar epithelial cells (Baskerville et al., 2018).
Why Normal-Weight Horses Get Laminitis
A frequent question is why normal-weight horses develop insulin-mediated laminitis. Hyperinsulinemia in horses is not exclusively linked to obesity.
Risk Factors That Worsen the Pathway
Seasonal pasture dynamics are among the most significant amplifiers of post-prandial hyperinsulinemia. Cool nights followed by sunny days increase nonstructural carbohydrate accumulation in grasses, raising laminitis risk.
Early Recognition of Hyperinsulinemia
Because hyperinsulinemia often precedes clinical laminitis, proactive metabolic screening is essential. Monitoring insulin levels in horses with EMS or seasonal pasture exposure allows earlier intervention and reduces the likelihood of severe lamellar compromise.
Conclusion
Hyperinsulinemia in horses is a primary driver of endocrinopathic laminitis. Sustained elevations in insulin activate lamellar epithelial cells via insulin receptor signaling and the IGF-1 receptor laminitis pathway, leading to structural remodeling and weakening of the hoof laminae (Baskerville et al., 2018; Lane et al., 2017).
Frequently Asked Questions (FAQs)
Q1: Can a horse get laminitis even if it’s not overweight?
A: Yes. Hyperinsulinemia can occur in normal-weight horses, particularly when post-prandial insulin responses are exaggerated (Durham et al., 2019).
Q2: How high does insulin need to be to cause laminitis?
A: Sustained elevations above physiological norms significantly increase laminitis risk, especially when repeated over time (Durham et al., 2019).
Q3: What is the role of the IGF-1 receptor in lamellar damage?
A: High insulin concentrations can activate lamellar epithelial cells through IGF-1 receptor–involving mechanisms, triggering structural remodeling and weakening of lamellar attachments (Baskerville et al., 2018; Lane et al., 2017).
Call to Action
Monitor your horse’s insulin levels regularly if risk factors such as equine metabolic syndrome, seasonal pasture exposure, or regional adiposity are present. Share this article with other horse owners and equine professionals to increase awareness of hyperinsulinemia in horses and its role in laminitis. Explore further educational resources on EMS and safe feeding practices to reduce laminitis risk.
References
- Baskerville, C. L., Chockalingham, S., Harris, P. A., & Bailey, S. R. (2018). The effect of insulin on equine lamellar basal epithelial cells mediated by the insulin-like growth factor-1 receptor. PeerJ, 6, e5945.
- Carslake, H. B., Pinchbeck, G. L., Argo, C. M., Dugdale, A. H. A., & McGowan, C. M. (2024). Investigation of glucagon-like peptide-1 response to six oral carbohydrates in ponies. Research in Veterinary Science, 170, 105–113.
- Durham, A. E., Frank, N., McGowan, C. M., Menzies-Gow, N. J., Roelfsema, E., Vervuert, I., Feige, K., & Fey, K. (2019). ECEIM consensus statement on equine metabolic syndrome. Journal of Veterinary Internal Medicine, 33(2), 335–349.
- Fitzgerald, D. M., Spence, R. J., Stewart, Z. K., Prentis, P. J., Sillence, M. N., & de Laat, M. A. (2020). The effect of diet change and insulin dysregulation on the faecal microbiome of ponies. Journal of Experimental Biology, 223(7), jeb219154.
- Giles, S. L., Rands, S. A., Nicol, C. J., & Harris, P. A. (2014). Obesity prevalence and associated risk factors in outdoor living domestic horses and ponies. PeerJ, 2, e299.
- Grenager, N. S. (2021). Endocrinopathic laminitis. Veterinary Clinics of North America: Equine Practice, 37(3), 619–638.
- Kirkwood, N. C., Hughes, K. J., & Stewart, A. J. (2022). Pituitary pars intermedia dysfunction (PPID) in horses. Veterinary Sciences, 9(10), 556.
