08/23/2025
Equine Metabolic Syndrome (EMS)
Brian S. Burks, DVM
Diplomate, ABVP
Board Certified Equine Specialist
Equine metabolic syndrome is known for its multiple risk factors for laminitis due to insulin dysregulation (ID), genetic predisposition, and obesity. Internal adipose tissue—visceral and retroperitoneal—appears to experience the strongest pathologic disruptions.
Affected animals typically are obese, with increased condition score overall and increased regional adiposity in the neck and tailhead regions. Laminitis, both chronic and acute, is common. Hyperinsulinemia with normal blood glucose concentrations (insulin resistance) is the primary clinical pathologic finding. Other associated signs include infertility, altered ovarian activity, and increased appetite. Other laboratory findings include hypertriglyceridemia, increased serum concentrations of leptin, and arterial hypertension.
At one time, this cluster of clinical signs was referred to as hypothyroidism, but thyroid responses are normal and thyroidectomized horses do not develop obesity or laminitis. EMS/ID is the result of an inability to properly metabolize carbohydrate, and many horses have exaggerated glucose and insulin responses to oral carbohydrate. Any abnormality in carbohydrate metabolism in horses is called insulin dysregulation.
EMS develops in horses five to 16 years old, in horses, donkeys, and ponies. It is most common in ponies, Saddlebreds, Tennessee Walking Horses, Paso Finos, Morgans, Mustangs, and Quarter horses, but is infrequently diagnosed n Thoroughbreds and Standardbreds.
The underlying reason why some horses develop equine metabolic syndrome and others do not is not known. There appears to be a genetic disposition. Affected horses may possess a “thrifty” gene that enabled their ancestors to survive in harsh environments. This increased efficiency of energy metabolism became maladaptive in modern environments with plentiful, nutrient-dense feedstuffs.
EMS may be a predisposing factor for pituitary pars intermedia dysfunction (PPID; also called equine Cushing’s disease). Both endocrine disorders can occur concurrently in middle-aged and older horses. Horses with EMS should therefore be monitored to detect the onset of PPID.
Affected equids are typically obese, with a body condition score >6/9. There is regional adiposity with a cresty neck (the nuchal ligament is full of fat and can get large enough to ‘fracture’ and fall to one side), fat deposition over the ribs, topline, and tail head. There may be increased fat deposition in the prepuce and mammary glands.
Adipocyte size and hypertrophy occur with excess calorie intake and these characteristics are associated with insulin resistance and dyslipidemia in humans. EMS horses experienced marked adipocyte hypertrophy and subsequent inflammation and circulating cytokines. Marked leptin gene expression also occurs in EMS horses and is related to adipocyte volume.
Acute and chronic laminitis are common. Horses brought in for evaluation with no previous history of laminitis often show evidence of prior episodes, such as abnormal hoof growth rings and radiographic evidence of third phalanx rotation or pedal osteitis. Laminitis may occur secondary to ingestion of feeds high in soluble carbohydrates, either in the form of lush pasture or high-carbohydrate hays and supplements. This can result in bouts of laminitis developing in the spring, when new pasture growth appears, and in the fall, when night temperatures are below freezing.
The common denominators behind many of the signs associated with EMS appear to be increased adiposity, insulin resistance, and hyperinsulinemia. When obesity develops, adipose tissues elaborate leptin and other adipokines as well as tumor necrosis factor and other inflammatory mediators. Increased fat stores in the liver may also predispose to insulin resistance due to down-regulation of insulin receptors.
Hyperinsulinemia leads to laminitis in horses and ponies. Insulin has vasoregulatory actions. Insulin resistance can decrease nitric oxide production and promote vasoconstriction. Altered glucose and insulin levels may also lead to altered epidermal cell function and glucose uptake by epidermal laminar cells. These effects predispose horses with EMS to develop laminitis.
Affected horses often do not lose weight without extreme food restriction, and obesity is exacerbated by laminitis, which limits exercise. Horses have increased appetites and will eat continually.
The development of obesity leads to increased glucocorticoid production by omental adipocytes, contributing to insulin resistance. This may be a survival mechanism as wild horses and ponies are able to gain weight during the summer months when forage is plentiful but lose weight over the winter during harsh periods when forage does not grow. This response maintains blood glucose for the CNS, and this may confer an advantage over others during times of food deprivation. Horses and ponies are commonly fed energy-rich rations that exceed requirements for exercise and survival. These diets also have potential complications of colic, typhlocolitis, osteochondrosis, and laminitis. Mares that suffer malnutrition for even short periods may cause damage to fetal cells, leading to the development of equine metabolic disease as an adult.
Diagnosis requires documenting insulin resistance and excluding PPID. Clinical signs alone are not enough to make a diagnosis. Even without a history of laminitis, the feet should be carefully examined and radiographed.
Many conditions can affect blood glucose and insulin levels, including diet, pain, and stress. Testing should be delayed in horses with laminitis until the animal is relatively pain free and should be performed in a controlled manner with minimal stress.
Blood glucose concentrations are within reference range or slightly increased with EMS. Persistent hyperglycemia should lead to PPID testing. Insulin measurement should follow a 6-8 hour fast, leaving only one flake of hay overnight. A blood insulin concentration >20 μU/mL is suggestive of insulin resistance.
Documentation of insulin dysregulation requires an oral sugar test; some horses are normal in all respects except for the ability to handle an oral carbohydrate load. The OST is performed by fasting the horse for 3-12 hours and then giving an oral dose of corn syrup at 0.15-0.45 mL/kg. Blood should be collected at 60 or 90 minutes after administration of the corn syrup for insulin determination. An insulin concentration >60 mU/L is abnormal.
To determine whether insulin can stimulate normal glucose uptake by peripheral tissues, an insulin tolerance test can be performed. This is accomplished by collecting a baseline blood sample for glucose concentration, giving regular human recombinant insulin, and then collecting a second blood sample for glucose concentration 30 minutes later. A second blood glucose concentration that does not decrease to 50% or less of the baseline value indicates insulin resistance.
Tests for PPID such as measuring endogenous ACTH concentration or thyroid releasing hormone response test are normal in horses with EMS. Positive results indicate that the horse is concurrently affected by EMS and PPID, which can occur in older horses. Detection of PPID is important, because it is thought that PPID exacerbates insulin resistance in horses affected by EMS.
Treatment for equine metabolic syndrome involves dietary management and, if diet and exercise is not sufficient to treat the condition, medical therapy. Correction of the diet may be all that is needed to return the horse to normal body weight. Total caloric intake should be reduced.
Forced activity is helpful, but despite this, weight can be difficult to lose. When diet and exercise are not sufficient, thyroxine or metformin may be used to improve insulin sensitivity. Thyroxine will also accelerate weight loss. The latter does not work well in horses, as it is poorly absorbed in horses. The longterm efficacy and safety of metformin has not been established in horses. If it is used, blood glucose should be carefully monitored. Use of metformin should be discontinued if hypoglycemia is documented.
The nonstructural carbohydrate (NSC) content of forage should be determined by feed analysis. This can be calculated by adding starch and water-soluble carbohydrate percentages. Ideally, NSC should comprise < 10% of the hay dry matter, and it should never exceed 16%. Soaking hay in water for 60 minutes has been recommended to lower water-soluble carbohydrate concentrations, but the actual amount reduced is extremely variable; hence, this is not a reliable method to produce a low-NSC forage.
Because there is insulin resistance, removing carbohydrates from the diet is essential. This means that all sweet feed products, including many complete feeds, should not be fed. Typical sweet feeds contain 80-90% simple sugars. Oats are approximately 60-80% simple sugar. Reducing the nonstructural carbohydrates to less than 15% is extremely helpful in improving the clinical signs of affected horses. Often grain is only fed because of the owner’s perception that it is a necessary part of the diet; however, simply removing grain and maintaining the horse on good quality grass hay often helps tremendously. In some cases, grass hay with
