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Home / Equine Research Bank / Equine Vet J / Glucose transport in the equine hoof.
Equine veterinary journal2011; 43(2); 196-201; doi: 10.1111/j.2042-3306.2010.00127.x

Glucose transport in the equine hoof.

Abstract: Several conditions associated with laminitis in horses are also associated with insulin resistance, which represents the failure of glucose uptake via the insulin-responsive glucose transport proteins in certain tissues. Glucose starvation is a possible mechanism of laminitis, but glucose uptake mechanisms in the hoof are not well understood. Objective: To determine whether glucose uptake in equine lamellae is dependent on insulin, to characterise the glucose transport mechanism in lamellae from healthy horses and ponies, and to compare this with ponies with laminitis. Methods: Study 1 investigated the effects of insulin (300 µU/ml; acute and 24 h) and various concentrations of glucose up to 24 mmol/l, on 2-deoxy-D-[2,6-(3)H] glucose uptake in hoof lamellar explants in vitro. Study 2 measured the mRNA expression of GLUT1 and GLUT4 transport proteins by PCR analysis in coronary band and lamellar tissue from healthy horses and ponies, ponies with insulin-induced laminitis, and ponies suffering from chronic laminitis as a result of equine Cushing's syndrome. Results: Glucose uptake was not affected by insulin. Furthermore, the relationship between glucose concentration and glucose uptake was consistent with an insulin-independent glucose transport system. GLUT1 mRNA expression was strong in brain, coronary band and lamellar tissue, but was weak in skeletal muscle. Expression of GLUT4 mRNA was strong in skeletal muscle, but was either absent or barely detectable in coronary band and lamellar tissue. Conclusions: The results do not support a glucose deprivation model for laminitis, in which glucose uptake in the hoof is impaired by reduced insulin sensitivity. Hoof lamellae rely on a GLUT1-mediated glucose transport system, and it is unlikely that GLUT4 proteins play a substantial role in this tissue. Conclusions: Laminitis associated with insulin resistance is unlikely to be due to impaired glucose uptake and subsequent glucose deprivation in lamellae.
© 2010 EVJ Ltd.
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Publication Date: 2011-05-20 PubMed ID: 21592215DOI: 10.1111/j.2042-3306.2010.00127.xGoogle Scholar: Lookup
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  • 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 how glucose transport functions in the equine hoof. It particularly focuses on understanding the connection between conditions like laminitis (common in horses) and insulin resistance that causes a decrease in the uptake of glucose in particular tissues in the horses’ body. The study also aims to characterize the glucose transport method in the lamellae of healthy horses and ponies compared to those with laminitis.

Research Methodology

  • The study was conducted in two parts. The first part involved studying the effects of insulin and varying concentrations of glucose on glucose uptake in the hoof lamellar explants in an in vitro setup. This helped to determine if glucose uptake in equine lamellae is dependent on insulin.
  • The second part of the study included estimating the mRNA expression of the GLUT1 and GLUT4 glucose transport proteins in the coronary band and lamellar tissue from healthy horses and ponies. These results were compared with similar data from ponies with insulin-induced laminitis and ponies with chronic laminitis resulting from equine Cushing’s syndrome.

Findings of the Research

  • The insulin presence did not affect the glucose uptake, indicating the existence of an insulin-independent glucose transport system.
  • GLUT1, one of the transport proteins, had strong mRNA expression in the brain, coronary band, and lamellar tissue but remained weak in the skeletal muscle. This suggests that hoof lamellae majorly rely on the GLUT1-mediated glucose transport system.
  • Conversely, the expression of GLUT4 mRNA was strongly detected in skeletal muscle, whereas its presence was almost negligible in coronary bands and lamellar tissue. This implies that GLUT4 proteins do not contribute substantially to glucose transport in these tissues.

Conclusion of the Research

  • The findings refute the glucose deprivation model for laminitis, which proposes that a reduced insulin sensitivity impairs glucose uptake in the hoof causing deprivation, leading to laminitis.
  • The research suggests that laminitis, linked to insulin resistance, is probably not a result of hampered glucose uptake and the subsequent glucose deprivation in the lamellae.

Cite This Article

APA
Asplin KE, Curlewis JD, McGowan CM, Pollitt CC, Sillence MN. (2011). Glucose transport in the equine hoof. Equine Vet J, 43(2), 196-201. https://doi.org/10.1111/j.2042-3306.2010.00127.x

Publication

Equine veterinary journal
ISSN: 0425-1644
NlmUniqueID: 0173320
Country: United States
Language: English
Volume: 43
Issue: 2
Pages: 196-201

Researcher Affiliations

Asplin, K E
  • School of Veterinary Science, The University of Queensland, Australia. asplin@nottingham.ac.uk
Curlewis, J D
    McGowan, C M
      Pollitt, C C
        Sillence, M N

          MeSH Terms

          • Animals
          • Biological Transport, Active / physiology
          • Foot Diseases / metabolism
          • Foot Diseases / veterinary
          • Gene Expression Regulation / physiology
          • Glucose / metabolism
          • Glutamate Plasma Membrane Transport Proteins / genetics
          • Glutamate Plasma Membrane Transport Proteins / metabolism
          • Horses / metabolism
          • Inflammation / metabolism
          • Inflammation / veterinary
          • Mephitidae / metabolism
          • Time Factors
          • Tissue Culture Techniques

          Citations

          This article has been cited 10 times.
          1. Menzies-Gow NJ, Knowles EJ. Sodium-glucose transport protein 2 inhibitor use in the management of insulin dysregulation in ponies and horses. J Vet Pharmacol Ther 2025 Jan;48 Suppl 1(Suppl 1):31-40.
            doi: 10.1111/jvp.13470pubmed: 38984777google scholar: lookup
          2. Stefaniuk-Szmukier M, Piórkowska K, Ropka-Molik K. Equine Metabolic Syndrome: A Complex Disease Influenced by Multifactorial Genetic Factors. Genes (Basel) 2023 Jul 27;14(8).
            doi: 10.3390/genes14081544pubmed: 37628596google scholar: lookup
          3. Stokes SM, Burns TA, Watts MR, Bertin FR, Stefanovski D, Medina-Torres CE, Belknap JK, van Eps AW. Effect of digital hypothermia on lamellar inflammatory signaling in the euglycemic hyperinsulinemic clamp laminitis model. J Vet Intern Med 2020 Jul;34(4):1606-1613.
            doi: 10.1111/jvim.15835pubmed: 32583504google scholar: lookup
          4. Watts MR, Hegedus OC, Eades SC, Belknap JK, Burns TA. Association of sustained supraphysiologic hyperinsulinemia and inflammatory signaling within the digital lamellae in light-breed horses. J Vet Intern Med 2019 May;33(3):1483-1492.
            doi: 10.1111/jvim.15480pubmed: 30912229google scholar: lookup
          5. Durham AE, Frank N, McGowan CM, Menzies-Gow NJ, Roelfsema E, Vervuert I, Feige K, Fey K. ECEIM consensus statement on equine metabolic syndrome. J Vet Intern Med 2019 Mar;33(2):335-349.
            doi: 10.1111/jvim.15423pubmed: 30724412google scholar: lookup
          6. Reisinger N, Schaumberger S, Nagl V, Hessenberger S, Schatzmayr G. Concentration Dependent Influence of Lipopolysaccharides on Separation of Hoof Explants and Supernatant Lactic Acid Concentration in an Ex Vivo/In Vitro Laminitis Model. PLoS One 2015;10(11):e0143754.
            doi: 10.1371/journal.pone.0143754pubmed: 26599864google scholar: lookup
          7. de Laat MA, Gruntmeir KJ, Pollitt CC, McGowan CM, Sillence MN, Lacombe VA. Hyperinsulinemia Down-Regulates TLR4 Expression in the Mammalian Heart. Front Endocrinol (Lausanne) 2014;5:120.
            doi: 10.3389/fendo.2014.00120pubmed: 25101057google scholar: lookup
          8. Lacombe VA. Expression and regulation of facilitative glucose transporters in equine insulin-sensitive tissue: from physiology to pathology. ISRN Vet Sci 2014;2014:409547.
            doi: 10.1155/2014/409547pubmed: 24977043google scholar: lookup
          9. Burns TA, Watts MR, Weber PS, McCutcheon LJ, Geor RJ, Belknap JK. Effect of dietary nonstructural carbohydrate content on activation of 5'-adenosine monophosphate-activated protein kinase in liver, skeletal muscle, and digital laminae of lean and obese ponies. J Vet Intern Med 2014 Jul-Aug;28(4):1280-8.
            doi: 10.1111/jvim.12356pubmed: 24750267google scholar: lookup
          10. Gauff F, Patan-Zugaj B, Licka TF. Hyperinsulinaemia increases vascular resistance and endothelin-1 expression in the equine digit. Equine Vet J 2013 Sep;45(5):613-8.
            doi: 10.1111/evj.12040pubmed: 23489109google scholar: lookup
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