Equine laminitis: ultrastructural lesions detected in ponies following hyperinsulinaemia

• Published in: Equine veterinary journal Vol. 41; no. 7; p. 671
• Main Authors: Nourian, A R, Asplin, K E, McGowan, C M, Sillence, M N, Pollitt, C C
• Format: Journal Article
• Language: English
• Published: United States 01.09.2009
• Subjects: Animals; Foot Diseases - chemically induced; Foot Diseases - pathology; Foot Diseases - veterinary; Hoof and Claw - pathology; Hoof and Claw - ultrastructure; Horse Diseases - chemically induced; Horse Diseases - pathology; Horses; Inflammation - chemically induced; Inflammation - pathology; Inflammation - veterinary; Insulin - toxicity; Microscopy, Electron, Transmission
• ISSN: 0425-1644
• DOI: 10.2746/042516409X407648

Anatomical changes in the hoof lamellar tissue induced by prolonged hyperinsulinaemia have not been described previously. Analysis of the induced lesions may promote understanding of hyperinsulinaemic laminitis pathogenesis and produce clinical benefit. To use light and transmission electron microscopy (TEM) to document hoof lamellar lesions in ponies clinically lame after prolonged hyperinsulinaemia. Nine clinically normal, mature ponies were allocated randomly to either a treatment group (n = 5) or control group (n = 4). The treatment group received insulin via a modified, prolonged euglycaemic hyperinsulinaemic clamp technique (EHCT) and were subjected to euthanasia when clinical signs of Obel grade II laminitis occurred. The control group was sham treated with an equivalent volume of 0.9% saline and killed at 72 h. Lamellar tissues of the right front feet were harvested and processed for TEM. Lamellae from insulin treated ponies were attenuated and elongated with many epidermal basal cells (EBC) in mitosis. Unlike carbohydrate induced laminitis in horses there was no global separation at the lamellar dermal/epidermal interface among ponies. Sporadic EBC basement membrane (BM) separation was associated with the proximity of infiltrating leucocytes. In 2 ponies, the lamellar BM was thickened. The number of hemidesmosomes/microm of BM was decreased in all insulin treated ponies. Prolonged hyperinsulinaemia causes unique lamellar lesions normally characteristic of acute and chronic laminitis. Lamellar proliferation may be an insulin effect through its mitogenic pathway. Aberrant lamellar mitosis may lengthen and weaken the lamellar, distal phalanx attachment apparatus and contribute to the clinical signs that developed. The study shows that insulin alone, in higher than normal circulating concentrations, induces profound, changes in lamellar anatomy. Medical control of insulin resistance and hyperinsulinaemia may ameliorate lesions and produce clinical benefit.