Analyze Diet
Domestic animal endocrinology2019; 69; 30-34; doi: 10.1016/j.domaniend.2019.04.004

Ultrastructural examination of basement membrane pathology in horses with insulin-induced laminitis.

Abstract: The third phalanx of the equine digit is suspended within the hoof capsule by a specialized interdigitating dermoepidermal layer called the lamellae, which fails during laminitis. Pathology of the basement membrane (BM), which interfaces epidermis and dermis, is evident during acute laminitis. However, BM damage appears to be less prevalent in ponies with the insulin-associated form of laminitis. The aim of the present study was to investigate changes to the ultrastructure and morphometry of the lamellar BM in the acute phase of insulin-induced laminitis in horses. Lamellar tissue from the left forefoot of 3 horses with acute hyperinsulinemic laminitis was examined with transmission electron microscopy and compared with tissue from normal horses. Lamellar BM width and hemidesmosome (HD) density were assessed every 5 μm along ∼200 μm of secondary epidermal lamellar BM. The BM zone of treated horses was extensively disorganized with loss of uniformity of the lamina lucida and lamina densa, fragmentation and disorientation of HDs, and cytoskeletal disengagement of the HDs. The mean (±SD) lamellar BM was twice as wide in treated (0.25 ± 0.05 μm), compared with control (0.14 ± 0.02 μm), horses. The HD density (HDs/μm) was reduced by half in the treatment group (1.88 ± 0.37), compared with controls (3.6 ± 0.13). The reduced number of HDs in horses with laminitis may contribute to the weakening of the dermoepidermal junction and lamellar failure. Disassembly of HDs during excessive cellular proliferation, secondary to hyperinsulinemia, may account for HD loss. Further investigation of the underlying etiopathogenesis of BM dysfunction during hyperinsulinemic laminitis in horses may facilitate an improved understanding of the disease.
Publication Date: 2019-05-16 PubMed ID: 31280023DOI: 10.1016/j.domaniend.2019.04.004Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research article investigates the changes in the ultrastructure and morphometry of the lamellar basement membrane in horses during the acute phase of insulin-induced laminitis.

Introduction and Aim

  • The research focuses on laminitis, a disease affecting horses where the lamellae – a dermoepidermal layer in the hooves – fails. The basement membrane (BM), an interface between the epidermis and dermis, shows signs of pathology during acute laminitis.
  • Interestingly, there seems to be less basement membrane damage in ponies with insulin-associated laminitis. The aim of the study, therefore, was to explore changes in the lamellar basement membrane’s ultrastructure and morphometry during the acute phase of insulin-induced laminitis in horses.

Methods

  • The researchers examined lamellar tissue from the left forefoot of three horses with acute hyperinsulinemic laminitis. This was then compared to tissue from normal horses.
  • The team used transmission electron microscopy to investigate the lamellar BM width and the density of hemidesmosome (HD), a type of protein structure. These assessments were made every 5 micrometers along approximately 200 micrometers of secondary epidermal lamellar BM.

Results

  • The findings indicate extensive disorganization in the BM zone of treated horses, marked by a loss of uniformity of the lamina lucida and lamina densa, fragmentation and disorientation of HDs, and cytoskeletal disengagement of the HDs.
  • The average lamellar BM width was found to be twice as large in treated horses as in the control group. Similarly, the average HD density was halved in the treatment group compared to the controls.
  • The reduced number of HDs may contribute to the weakening of the dermoepidermal junction and lamellar failure.

Conclusion and Further Implications

  • The disassembly of HDs during excessive cellular proliferation, secondary to hyperinsulinemia, could explain the loss of HDs.
  • Overall, more research into the cause and effect of BM dysfunction during hyperinsulinemic laminitis in horses could lead to a better understanding of the disease and potentially improved treatments.

Cite This Article

APA
de Laat MA, Pollitt CC. (2019). Ultrastructural examination of basement membrane pathology in horses with insulin-induced laminitis. Domest Anim Endocrinol, 69, 30-34. https://doi.org/10.1016/j.domaniend.2019.04.004

Publication

ISSN: 1879-0054
NlmUniqueID: 8505191
Country: United States
Language: English
Volume: 69
Pages: 30-34
PII: S0739-7240(19)30027-X

Researcher Affiliations

de Laat, M A
  • School of Veterinary Science, The University of Queensland, Gatton, Queensland, Australia. Electronic address: melody.delaat@qut.edu.au.
Pollitt, C C
  • School of Veterinary Science, The University of Queensland, Gatton, Queensland, Australia.

MeSH Terms

  • Animals
  • Basement Membrane / ultrastructure
  • Case-Control Studies
  • Foot Diseases / chemically induced
  • Foot Diseases / veterinary
  • Hoof and Claw / pathology
  • Horse Diseases / chemically induced
  • Horse Diseases / pathology
  • Horses
  • Inflammation / chemically induced
  • Inflammation / pathology
  • Inflammation / veterinary
  • Insulin / toxicity

Citations

This article has been cited 2 times.
  1. Kirkwood NC, Hughes KJ, Stewart AJ. Pituitary Pars Intermedia Dysfunction (PPID) in Horses. Vet Sci 2022 Oct 10;9(10).
    doi: 10.3390/vetsci9100556pubmed: 36288169google scholar: lookup
  2. Stokes SM, Stefanovski D, Bertin FR, Medina-Torres CE, Belknap JK, van Eps AW. Plasma amino acid concentrations during experimental hyperinsulinemia in 2 laminitis models. J Vet Intern Med 2021 May;35(3):1589-1596.
    doi: 10.1111/jvim.16095pubmed: 33704816google scholar: lookup