Equine laminitis: Ultrastructural lesions detected in ponies following hyperinsulinaemia

Nourian, A. R., Asplin, K. E., McGowan, C. M., Sillence, M. N. and Pollitt, C. C. (2009) Equine laminitis: Ultrastructural lesions detected in ponies following hyperinsulinaemia. Equine Veterinary Journal, 41 7: 671-677. doi:10.2746/042516409X407648


Author Nourian, A. R.
Asplin, K. E.
McGowan, C. M.
Sillence, M. N.
Pollitt, C. C.
Title Equine laminitis: Ultrastructural lesions detected in ponies following hyperinsulinaemia
Journal name Equine Veterinary Journal   Check publisher's open access policy
ISSN 0425-1644
2042-3306
Publication date 2009-09
Sub-type Article (original research)
DOI 10.2746/042516409X407648
Volume 41
Issue 7
Start page 671
End page 677
Total pages 7
Place of publication Hoboken, NJ, United States
Publisher John Wiley & Sons
Language eng
Formatted abstract
Reasons for performing study:
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.

Objectives:

To use light and transmission electron microscopy (TEM) to document hoof lamellar lesions in ponies clinically lame after prolonged hyperinsulinaemia.

Methods:
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.

Results:

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/μm of BM was decreased in all insulin treated ponies.

Conclusions:

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.

Potential relevance:
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.
Keyword Horse
Laminitis
Insulin
Ultrastructural
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: ERA 2012 Admin Only
School of Veterinary Science Publications
 
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Created: Sun, 13 Dec 2009, 00:06:12 EST