“Metabolic syndrome” (MS), Cushing’s disease, insulin resistance, glucose intolerance, and “glycemic indices” of feeds and foods have gotten a lot of attention recently in both the human and equine media. These terms have been used in reference to horses that have increased incidence of laminitis (adult horses) and developmental orthopedic disease (growing horses). The terms are taken from the human literature, where they have very specific clinical and scientific definitions that do not always coincide directly with the equine problems. Before we can understand the equine syndrome(s) and how to treat them, we first need to define the terms and recognize the differences between horses and other species, such as humans and dogs.

TERMINOLOGY

• Insulin resistance (IR) is a reduced sensitivity of the body’s cells to insulin’s facilitation of glucose uptake, resulting in higher than normal insulin release in response to a carbohydrate meal. Blood glucose concentrations may be normal (compensated) or elevated (hyperglycemia, uncompensated glucose intolerance). This has been well defined in horses and appears to coincide closely with what is seen in humans.
  
  

• Cushing’s disease is classically due to tumors in the pituitary gland in humans and dogs. These tumors cause unregulated secretion of adrenocorticotrophic hormone (ACTH) that stimulates increased cortisol release from the adrenal gland, mimicking a stress response. The higher than normal blood concentrations of cortisol contribute to the classic clinical signs of hyperglycemia, IR, excessive thirst (polydypsia) and urination (polyuria) and hair loss. In horses the syndrome is associated not only with IR, polyuria, and polydypsia, but also reproductive failure in mares and laminitis. Instead of hair loss, horses that have pituitary tumors tend to retain their long, shaggy, winter coats throughout the year. Though tumors are usually present, they tend to be in a different location in the horse’s pituitary gland than in other species. Therefore, it has been proposed that this syndrome in horses should be called “pituitary dysfunction” instead due to the dissimilarities from classic Cushing’s disease in other species.
  
  

• Metabolic syndrome (MS) is characterized by compensated or uncompensated insulin resistance and hypertension in humans that do not have pituitary tumors, and is often, but not always, associated with obesity. Hypertension has not been documented in horses “diagnosed” as having MS, but they are prone to laminitis, which involves hypertensive changes in the blood supply to the hoof and are frequently obese. There is disagreement as to whether non-obese IR horses are truly comparable to humans with MS.
  
  

• Glycemic index of foods is defined as the glucose response to a particular food compared to that of a “standard meal” of white bread in humans. In equine studies, oats, starch/sugar solutions (2 gm/kg) and sweet feeds have variously been used as the “standard meal.” Since different standards have been used it is hard to establish the actual glycemic index of horse feeds.

DIAGNOSIS OF MS AND IR

Recently in horses, the only basis used for diagnosis of MS, Cushing’s disease or IR has been the presence of high insulin (hyperinsulinemia) and/or glucose (hyperglycemia) in a single blood sample. This can be grossly inaccurate and misleading. The mistaken diagnosis leads to unwarranted and usually untested recommendations that not only do not help the horse, but also place a huge financial and emotional burden on the owners.

Hyperinsulinemia, which is defined as an unusually high blood or plasma insulin concentration, with or without hyperglycemia, is common in horses. Pituitary dysfunction and obesity can cause IR and both are correlated with an increased risk of laminitis. In every study of insulin responses in horses for the past twenty years, at least one of the research animals has had exaggerated insulin responses and was reported separately, as an “outlier.” However, many of these hyperinsulinemic horses have been clinically normal. Therefore, every obese horse is not necessarily hyperinsulinemic, nor does every hyperinsulinemic horse have an increased risk of laminitis. Hyperinsulinemia has been correlated with the presence of OCD (osteochondrosis dissecans) lesions in weanlings less than 12 months of age; however, cause and effect have not been proven. There is no agreement at this time in the scientific community as to exactly how high an insulin concentration has to be for a horse to be considered “hyperinsulinemic” or IR.

Insulin resistance is ideally documented by hyperglycemic or euglycemic insulin “clamp” techniques. “Clamp” techniques involve infusing both insulin and glucose intravenously and, via frequent sampling and complex mathematical models, the amount of insulin required to reduce artificially high blood glucose (hyperglycemic clamp) or maintain (euglycemic clamp) blood glucose constant is calculated. These are direct measures of the cellular sensitivity and are considered to be the “gold standard” for diagnostic purposes; however very few clinics or even research centers are equipped to run them.

Simpler tests of insulin sensitivity are to administer, either orally or intravenously, a standardized glucose challenge and measure the glucose and insulin responses. Either peak responses or area under the response curve are calculated and compared to responses of horses considered to be “normal.” The responses, however, are influenced by a variety of factors such as plasma cortisol concentrations, time of day, diet to which the horse was adapted and even season of the year.

If you take a single blood sample without the above challenges, the glucose/insulin results will be meaningless unless you know:

• When the animal was last fed (glucose/insulin remains high for up to 4 hours after a meal of grain).

• Type of feed the horse recently ate (high sugar/starch feeds would cause greater responses than high fat/fiber concentrates or forage only ration).

• Ration to which it was adapted (horses on predominantly hay diets will have a lower insulin response to a meal of grain or glucose challenge than those adapted to high grain diets).

• Time of day and level of stress (morning responses are higher than those in the evening in unstressed horses due to normal diurnal fluctuations in cortisol).

Apparently abnormal glucose/insulin results should be followed by further, more definitive tests before instituting drug or drastic dietary measures.

FEEDING MS AND IR HORSES

If a definitive diagnosis of MS or IR is made, grain based feeds should be eliminated from the horse’s ration as much as possible. Since many of these horses will be obese, weight reduction is usually desirable and can be accomplished by limiting the horse to 1.5 % to 2.0 % of its body weight in grass hay divided into three or four feedings a day with free access to salt and water. Increasing exercise as much as possible will result in both weight loss and increased insulin sensitivity. Turn out in pastures or paddocks is not as effective as forced exercise such as lunging, working under saddle or in harness for over 15 minutes a day. Weight loss rations should not be high fat and fat supplementation should be avoided or discontinued at this time.

If additional feed is needed for maintenance once the desired weight loss is achieved, barley has consistently been reported to have the lowest glycemic response compared to other grains, regardless of the standards used. It should be rolled or flaked and fed in no more than 0.5% of the horse’s body weight per meal. Beet pulp also has a low glucose /starch content, as long as molasses has not been added, and can be fed soaked or in pelleted form for additional calories or as a carrier for supplements. There is no evidence that reduction of iron intake, chromium, or various herbal or “natural” supplements have any significant effect on insulin sensitivity in horses.

OTHER SUGGESTED READING

Harris P, Bailey S, Elliot J, Longland A. Countermeasures for pasture-associated laminitis in ponies and horses. J. Nutr. 2006;136:2114S-2121S.

Kronfeld D, Treiber K, Hess T, Boston R. Insulin resistance in the horse: definition, detection and dietetics. J. Anim. Sci. 2005;83:E22–31.

Longland A, Byrd B. Pasture nonstructural carbohydrates and equine laminitis. J Nutr. 2006;136:2099S-2102S.

Williams CA, Kronfeld DS, Staniar WB, Harris PA. Plasma glucose and insulin responses of Thoroughbred mares fed a meal high in starch and sugar or fat and fiber. J. Anim. Sci. 2001;79(8):2196-2201.

Published: August 2007

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