Equis ISSN 2398-2977

Equine metabolic syndrome

Synonym(s): EMS, Peripheral Cushing's syndrome, Pre-laminitis syndrome, Pre-laminitic metabolic syndrome

Contributor(s): Philip Johnson, Nicola Menzies-Gow, Ruth Morgan, Vetstream Ltd, Jo Ireland

Introduction

  • Cause: results from a combination of obesity, insulin resistance and a genetic predisposition, resulting in increased susceptibility to laminitis.
  • Signs: obesity, abnormal fat accumulation along crest and rump, recurrent/subacute/chronic laminitis, altered reproductive cycling in mares.
  • Diagnosis: fasting serum insulin concentrations, oral glucose test (OGT) or oral sugar test (OST), combined glucose-insulin tolerance test, rule out pituitary pars intermedia dysfunction.
  • Treatment: weight loss, exercise, treatment of laminitis as determined by the needs of individual patient. Pharmacological intervention, eg metformin.
  • Prognosis: treatment can control clinical signs; largely predicated by the severity of laminitic lameness and associated hoof degradation.
Print off the Owner factsheets on Body condition scoringEquine metabolic syndrome and Obesity - the fat horse to give to your clients.

Pathogenesis

Etiology

  • The syndrome of obesity and recurrent laminitis in horses has been likened to human metabolic syndrome.
  • In man:
    • Metabolic syndrome occurs in genetically susceptible individuals in combination with excessive dietary intake and inactivity over a prolonged period of time and is associated with obesity, insulin resistance and hypertension.
    • The human definition includes enhanced pro-inflammatory and pro-coagulability processes in the body; it also includes dyslipidemia (development of an atherogenic lipid profile; increased low density lipoproteins) and the result is an increased cardiovascular risk and diabetes.

There is controversy regarding definition of equine metabolic syndrome and its relationship to the human syndrome. Horses with EMS have been shown to demonstrate a pro-inflammatory state; there is some evidence of hypertension and dyslipidemia.

Predisposing factors

General

  • Genetic - ponies at greater risk; familial link reported in Dartmoor ponies   Dartmoor Pony  .
  • Dietary intake of calories excessive with respect to metabolic requirements (over time).
  • Obesity, especially thickening in the crest of the neck and thickening of the prepuce in geldings.
  • Inactivity.

Specific

  • Insulin resistance.
  • Genetic susceptibility.

Pathophysiology

  • The pathophysiology of EMS is extremely complex and not yet fully understood.
  • Adipocytes are endocrinologically active, not just fat stores.
  • Adipocytes, particularly omental adipocytes in humans, produce various hormones (adipokines, particularly adiponectin and leptin) that have systemic effects.
  • Adipocytes also possess the enzyme 11-b hydroxysteroid dehydrogenase (11-b HSD) that can convert inactive cortisol. In humans this enzyme is more active and abundant in obese people and those with metabolic syndrome.
  • The increased concentrations of cortisol and the adipokines antagonize the effects of insulin. This results in circulating hyperglycemia that is toxic to cells that do not rely on insulin to stimulate cellular uptake of glucose. The vascular endothelial cells are particularly susceptible (glucotoxic endotheliopathy)   →   endothelial dysfunction. This may predispose to digital ischemia and hence laminitis, but this has yet to be determined.
  • Obesity also causes lipid accumulation within striated muscle fibers:
    • Lipid accumulation within muscle fibers is antagonistic to the action of insulin.
    • Skeletal muscle represents the major site of the action of insulin and the insulin-mediated disposition of glucose in the body.
    • Intramyocellular lipid accumulation represents an important link between the development of obesity and the pathogenesis of insulin resistance.
  • A state of hyperinsulinemia has been shown to result in laminitis but the mechanisms of this association are unknown. Hyperinsulinemia may affect blood vessel tone, resulting in an altered blood supply to the hoof.
  • Although there is substantial speculation, a satisfactory explanation for the risk of laminitis associated with insulin resistance does not presently exist.

Timecourse

  • Develops over a prolonged period of time due to need for development of obesity.

Epidemiology

  • Very limited robust epidemiological data regarding EMS.
  • Owner-reported prevalence of EMS is low despite high prevalence of obesity, hyperinsulinemia and laminitis, indicating a significant proportion of cases are undiganosed.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Morgan R A, Keen J A & McGowan C M (2015) Treatment of equine metabolic syndrome: a clinical case seriesEquine Vet J doi: 10.1111/evj.12445 PubMed.
  • Morgan R A, Keen J A & McGowan C M (2015) Equine metabolic syndrome.Vet Rec 177 (7), 173-179 PubMed.
  • Argo C M, Dugdale A H & McGowan C M (2015) Considerations for the use of restricted, soaked grass hay diets to promote weight loss in the management of equine metabolic syndrome and obesityVet J 206 (2), 170-177 PubMed
  • Karikoski N P et al (2015) Pathology of natural cases of equine endocrinopathic laminitis associated with hyperinsulinemiaVet Pathol 52 (5), 945-956 PubMed.
  • Karikoski N P et al (2014) Morphological and cellular changes in secondary epidermal laminae of horses with insulin-induced laminitisAm J Vet Res 75 (2), 161-168 PubMed.
  • Morgan R A, McGowan T W & McGowan C M (2014) Prevalence and risk factors for hyperinsulinaemia in ponies in Queensland, AustraliaAust Vet J 92 (4), 101-106 PubMed.
  • McGowan C M et al (2013) Dietary restriction in combination with a nutraceutical supplement for the management of equine metabolic syndrome in horsesVet J 196 (2), 153-159 PubMed
  • Rendle D I et al (2013) Effects of metformin hydrochloride on blood glucose and insulin responses to oral dextrose in horsesEquine Vet J 45 (6), 751-754 PubMed.
  • Tadros E M & Frank N (2013) Endocrine disorders and laminitis. Equine Vet Educ 25 (3), 152-162 VetMedResource.
  • de Laat M A et al (2010) Equine laminitis: induced by 48 h hyperinsulinaemia in Standardbred horses. Equine Vet J 42 (2), 129-135 PubMed.
  • de Laat M A et al (2010) Hyperinsulinemic laminitis.Vet Clin North Am Equine Pract 26 (2), 257-264 PubMed.
  • Frank N et al (2010) Equine Metabolic Syndrome. J Vet Intern Med 24 (3), 467-475 PubMed.
  • Tinworth K D et al (2010) Pharmacokinetics of metformin after enteral administration in insulin-resistant ponies. Am J Vet Res 71 (10), 1201-1206 PubMed.
  • Carter R A et al (2009) Prediction of incipient pasture-associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised and localised obesity in a cohort of ponies. Equine Vet J 41 (2), 171-178 PubMed.
  • Durham A E, Rendle D I & Newton J E (2008) The effect of metformin on measurements of insulin sensitivity and beta cell response in 18 horses and ponies with insulin resistanceEquine Vet J 40 (5), 493-500 PubMed.
  • Menzies-Gow N J (2007)Equine metabolic syndromeUK Vet 12 (3), 15-17 VetMedResource.
  • Treiber K H, Kronfeld D S, Hess T M, Boston R C & Harris P A (2005) Use of proxies and reference quintiles obtained from minimal model analysis for determination of insulin sensitivity and pancreatic beta-cell responsiveness in horses. Am J Vet Res 66, 21142121 PubMed
  • Johnson P J, Messer N T, Slight S H et al (2004) Endocrinopathic laminitis in horsesClin Tech Eq Pract (1), 45-56 ScienceDirect.
  • Johnson P J (2002) The equine metabolic syndrome peripheral Cushing's syndromeVet Clin North Am Equine Pract 18 (2), 271-293 PubMed.


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