Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses

Authors

  • M. A. De LAAT,

    1. Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Brisbane, Queensland 4072, Australia; Equine Division, Department of Clinical Veterinary Science, University of Liverpool, Neston, CH64 7TE, UK; and
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  • C. M. McGOWAN,

    1. Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Brisbane, Queensland 4072, Australia; Equine Division, Department of Clinical Veterinary Science, University of Liverpool, Neston, CH64 7TE, UK; and
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  • M. N. SILLENCE,

    1. Faculty of Science and Technology, Queensland University of Technology, Brisbane, Queensland 4001, Australia.
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  • C. C. POLLITT

    1. Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Brisbane, Queensland 4072, Australia; Equine Division, Department of Clinical Veterinary Science, University of Liverpool, Neston, CH64 7TE, UK; and
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Summary

Reasons for performing study: Hyperinsulinaemia is known to induce laminitis experimentally in healthy ponies with no history of the condition. Horses are more insulin sensitive than ponies and whether prolonged hyperinsulinaemia and euglycaemia would have a similar laminitogenic effect requires study.

Objectives: To determine if laminitis results when the prolonged euglycaemic hyperinsulinaemic clamp technique (p-EHC) is applied to clinically normal Standardbred horses, and to monitor hoof wall temperature seeking an association between vascular activity and laminitis development.

Methods: Eight young, clinically normal Standardbred horses were assigned into 4 pairs and within each pair, one was assigned randomly to either treatment (n = 4) or control (n = 4) groups. Treated horses received continuous infusions of insulin and glucose until clinical signs of laminitis developed, at which point the horses were subjected to euthanasia. Control horses received an equivalent volume of a balanced electrolyte infusion for the same period. Hoof wall surface temperature (HWST) was monitored continuously throughout the experimental period.

Results: All horses in the treatment group were calculated to have normal insulin sensitivity. All treated horses, and none in the control group, developed laminitis (P = 0.01). Pronounced digital pulses were a feature of the treatment group, while insignificant digital pulses occurred in control horses. HWST was higher and less variable in treated horses once hyperinsulinaemia was established.

Conclusions: Healthy Standardbred horses subjected to prolonged hyperinsulinaemia develop laminitis within 48 h, demonstrating that laminitis in horses can be triggered by insulin.

Potential relevance: Insulin resistance and the associated hyperinsulinaemia place horses and ponies at risk of developing laminitis. This study demonstrates a need for prompt management of the persistent hyperinsulinaemia seen in some endocrinopathies.

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