Biochemical indices of vascular function, glucose metabolism and oxidative stress in horses with equine Cushing’s disease.
Abstract: The mechanisms underlying the increased risk of laminitis in horses with equine Cushing's disease (ECD) are poorly understood. Objective: That abnormalities in glucose homeostasis, similar to those which cause microvascular dysfunction in human diabetics, contribute to development of laminitis in horses with ECD. Methods: Thirty-one aged horses were divided into 3 groups based on clinical signs and dexamethasone suppression testing (DST). Group 1 (n = 12) had clinical ECD as evidenced by hirsutism. Group 2 (n = 10) had a positive DST but no hirsutism. Group 3 (n = 9) were controls without ECD, with a negative DST and no clinical evidence of ECD. Biochemical indices of glucose metabolism, vascular function and oxidative stress were determined in single morning blood samples. Results: Group 1 had abnormalities in glucose homeostasis, including increased levels of glucose and insulin, compared to Groups 2 and 3. Groups 1 and 2 had significantly lower plasma thiol (PSH) levels and nonsignificantly lower albumin-corrected PSH levels than Group 3, consistent with oxidative stress. Conclusions: The observed abnormalities in glucose metabolism and oxidative stress could potentially contribute to development of laminitis in horses with ECD, by similar mechanisms to those that cause microvascular dysfunction in human diabetics. The absence of inter-group differences in the biochemical indices of vascular function precludes their use as preclinical diagnostic indicators of vascular dysfunction. The study also highlighted limitations in the premortem diagnosis of ECD.
Publication Date: 2004-05-19 PubMed ID: 15147129DOI: 10.2746/0425164044877215Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The article’s research delineates the investigation into mechanisms that lead to an escalated risk of laminitis in horses suffering Equine Cushing’s disease. Experiments revealed abnormalities in glucose metabolism and oxidative stress, potentially contributing to laminitis development, likening these mechanisms to those causing microvascular dysfunction in human diabetes.
Research Objective
- The primary objective of this study was to discern the abnormalities in glucose homeostasis that could be akin to those causing microvascular dysfunction in human diabetes. This dysfunction has been theorized to contribute to the onset of laminitis in horses diagnosed with Equine Cushing’s disease (ECD).
Research Methodology
- A total of 31 aged horses were examined and divided into 3 groups based on clinical signs and dexamethasone suppression testing (DST).
- Group 1, which consisted of 12 horses, was diagnosed with ECD, as evident through hirsutism. Group 2 (10 horses) had a positive DST without hirsutism signs. Group 3 was control group comprised of 9 horses without ECD, as confirmed through negative DST results and no clinical indications of ECD.
- The researchers then collected samples of the horse’s blood in the morning to determine the biochemical indices of glucose metabolism, vascular function, and oxidative stress.
Results
- Group 1 showed irregularities in glucose homeostasis, marked by elevated glucose and insulin levels as compared to Group 2 and 3.
- Group 1 and 2 displayed significantly reduced plasma thiol (PSH) levels and nonsignificantly lower albumin-corrected PSH levels in comparison to Group 3, indicative of oxidative stress.
Conclusion
- The detected irregularities in glucose metabolism and oxidative stress could potentially stimulate the development of laminitis in horses with ECD. This followed the similar mechanisms causing microvascular dysfunction in human diabetics.
- However, the lack of differences in the biochemical indices of vascular function among the groups halted their use as early diagnostic markers of vascular dysfunction.
- The findings also spotlighted limitations in diagnosing ECD before the horse’s death.
Cite This Article
APA
Keen JA, McLaren M, Chandler KJ, McGorum BC.
(2004).
Biochemical indices of vascular function, glucose metabolism and oxidative stress in horses with equine Cushing’s disease.
Equine Vet J, 36(3), 226-229.
https://doi.org/10.2746/0425164044877215 Publication
Researcher Affiliations
- Easter Bush Veterinary Centre, University of Edinburgh, Roslin, Midlothian EH25 9RG, UK.
MeSH Terms
- Adrenocorticotropic Hormone / blood
- Animals
- Blood Glucose / metabolism
- Cushing Syndrome / blood
- Cushing Syndrome / complications
- Cushing Syndrome / veterinary
- Foot Diseases / blood
- Foot Diseases / etiology
- Foot Diseases / veterinary
- Fructosamine / blood
- Hoof and Claw / blood supply
- Hoof and Claw / pathology
- Horse Diseases / blood
- Horse Diseases / etiology
- Horse Diseases / metabolism
- Horse Diseases / physiopathology
- Horses
- Inflammation / blood
- Inflammation / metabolism
- Inflammation / veterinary
- Insulin / blood
- Insulin / metabolism
- Oxidative Stress / physiology
- Random Allocation
- Risk Factors
- Sulfhydryl Compounds / blood
Citations
This article has been cited 4 times.- Horn R, Stewart AJ, Jackson KV, Dryburgh EL, Medina-Torres CE, Bertin FR. Clinical implications of using adrenocorticotropic hormone diagnostic cutoffs or reference intervals to diagnose pituitary pars intermedia dysfunction in mature horses. J Vet Intern Med 2021 Jan;35(1):560-570.
- Żak A, Siwińska N, Chełmecka E, Bażanów B, Romuk E, Adams A, Niedźwiedź A, Stygar D. Effects of Advanced Age, Pituitary Pars Intermedia Dysfunction and Insulin Dysregulation on Serum Antioxidant Markers in Horses. Antioxidants (Basel) 2020 May 21;9(5).
- Mancini A, Festa R, Di Donna V, Leone E, Littarru GP, Silvestrini A, Meucci E, Pontecorvi A. Hormones and antioxidant systems: role of pituitary and pituitary-dependent axes. J Endocrinol Invest 2010 Jun;33(6):422-33.
- Mancini A, Leone E, Silvestrini A, Festa R, Di Donna V, De Marinis L, Pontecorvi A, Littarru GP, Meucci E. Evaluation of antioxidant systems in pituitary-adrenal axis diseases. Pituitary 2010 Jun;13(2):138-45.
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