Also known as Peripheral Cushings Disease and Equine Syndrome X.
It is an illness affecting Equidae (horses and related animals).
This is an area of much new research and is increasingly believed to have a major role in conditions such as laminitis. Although many factors (including cortisol metabolism and adipocyte (fat cell) turnover) are involved, the primary cause is insulin resistance. This is similar to type II diabetes in humans, where the action of insulin is impaired, despite often elevated concentrations.
Ponies and horse breeds that evolved in relatively harsh environments with only sparse grass (such as domesticated Spanish Mustangs and Peruvian Pasos, among others),[1] tend to be more prone to EMS and insulin resistance, possibly as a survival mechanism (i.e. lay down fat when conditions are good). Such animals are sometimes called "easy keepers."
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In EMS, peripheral adipocytes (fat cells) synthesise adipokines which are analogous to cortisol, resulting in Cushings syndrome-like symptoms.[2] However, cortisol levels are grossly normal,[3] and there is no pituitary dysfunction. In addition, omental adipocytes may produce the enzyme 11β-hydroxysteroid dehydrogenase type 1, which "regenerates" active cortisol from its inactive metabolite, cortisone,[2] which may induce a form of Cushings whereby normal cortisol levels have an exaggerated action due to a longer systemic Half-life.
In addition, a hormone termed resistin has been shown to be produced in adipose tissue, which is a known cause for insulin resistance.[3]
EMS is also implicated in the development of laminitis;[4] however, recent research suggests that the situation is more complex, in that "compensated insulin resistance is essentially physiological and health sustaining", and only when this compensatory mechanism fails does laminitis ensue[5] - this may support the argument that EMS is an evolved survival trait.[6]
EMS horses tend to become obese very easily and, even when starved down, may have abnormal fat deposits in the neck, shoulders, loin, above the eyes and around the tail head, even when the rest of the body appears to be in normal condition. Some cases may become pot-bellied, perhaps polydipsic, acyclic and generally lethargic.[3][7]
Often, the initial presentation is as a laminitic displaying signs of Cushings, but with a normal pituitary-adrenal axis.[7]
The basis of treatment is managing the horse's adipocyte level - i.e., weight and obesity control by dietary restriction and exercise.[8] Substantial clinical improvement can be achieved with as little as 5-10% weight reduction.[6] In addition, antioxidant treatment (e.g. Vitamin E or Chromium supplementation) have been suggested.
Pharmacological treatments tend to be symptomatic. The condition cannot be cured, but can be managed. Some veterinarians have reported success with pergolide and cyproheptadine, although the mechanism of any such action is unclear.[2] Trilostane has also been used extensively as hydroxysteroid-dehydrogenase inhibitor, to prevent overproduction of cortisol.[9] Exogenous thyroid hormone administration has also been used, on the rationale that thyroid hormones facilitate insulin-mediated glucose absorption by cells - however, they also facilitate glucose uptake by the gut, and in depth cost/benefit studies have not as yet been published.[6]