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, Ruth Morgan, Vetstream Ltd, Jo Ireland, Nicola Menzies-Gow

Introduction

  • Cause: results from insulin dysregulation and is associated with an increased susceptibility to laminitis.
  • Signs: generalized obesity, regional adiposity (abnormal fat accumulation along crest and rump), recurrent/subacute/chronic laminitis, altered reproductive cycling in mares.
  • Diagnosis: resting serum insulin concentrations, oral glucose test (OGT) or oral sugar test (OST), combined glucose-insulin tolerance test or insulin tolerance test, rule out pituitary pars intermedia dysfunction.
  • Treatment: weight loss if overweight/obese, exercise, treatment of laminitis as determined by the needs of individual patient. Pharmacological intervention, eg metformin or levothyroxine.
  • Prognosis: treatment can control clinical signs; largely predicated by the severity of laminitic lameness and associated hoof degradation.
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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 not 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.
  • Epigenetic factors - in utero exposure to excessive or under nutrition switches on or off genes which affect metabolism later in life.
  • Microbiome - hindgut bacteria produce products that influence metabolic health.
  • Dietary intake of calories excessive with respect to metabolic requirements (over time).
  • Diet affects insulin sensitivity, eg high starch vs high fat.
  • Obesity, especially thickening in the crest of the neck and thickening of the prepuce in geldings.
  • Physical inactivity.
  • Exposure to endocrine disrupting chemicals.

Specific

  • Insulin dysregulation.
  • 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.
  • The increased concentrations of cortisol and the adipokines antagonize the effects of insulin. This results in circulating hyperinsulinemia. The mechanism by which insulin induces laminitis is still to be determined. There is evidence for a role for inappropriate stimulation of lamellar insulin like growth factor 1 (IGF-1) receptors and for endothelial dysfunction. 
  • Insulin dysregulation manifests in three forms namely resting hyperinsulinemia, an excessive insulin response to oral carbohydrate and peripheral (tissue) insulin resistance; an individual animal may have any combination of these manifestations.

Timecourse

  • Develops over a prolonged period of time.

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 undiagnosed.

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 48 (4), 422-426 PubMed.
  • Morgan R A, Keen J A & McGowan C M (2015) Equine metabolic syndromeVet 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, 2114-2121 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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