Fat, foundered horses: What is equine metabolic syndrome? (Proceedings)

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Fat, foundered horses: What is equine metabolic syndrome? (Proceedings)

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Apr 01, 2010

Middle-aged obesity (body condition score 7-9 on a scale of 1 to 9) accompanied by insidious-onset laminitis is a syndrome that has been recognized by equine practitioners for decades. Equine metabolic syndrome (EMS) is a recently coined name that has gained acceptance to describe this condition. Clinical signs of laminitis commonly develop while horses are grazing spring pasture but can also occur at other times of the year and in horses without pasture access. Affected horses tend to be aged between 10-to-20 years and there does not appear to be a sex predilection. Occasionally, the syndrome can occur in younger animals that have been overfed. Pony breeds, domesticated Spanish mustangs, Peruvian Pasos, Paso Finos, Andalusians, European Warmbloods, American Saddlebreds, Arabians, and Morgan horses are more commonly affected than Thoroughbreds, Standardbreds, and Quarter Horses. This breed disparity is supportive of a genetic predisposition. In the past, this syndrome was commonly attributed to hypothyroidism or pituitary pars intermedia dysfunction (PPID or classic equine Cushing's disease); however, most affected horses do not manifest additional clinical signs or endocrinologic test results to support these conditions. It is now recognized that insulin resistance is the primary endocrinopathy induced by obesity in EMS-affected horses. However, a number of additional metabolic and endocrinologic alterations can occur in affected equids making the pathophysiology of EMS an increasingly complex subject. Finally, a subgroup of EMS-affected equids may only have abnormal fatty deposits (e.g., a cresty neck or fat deposits behind the shoulders, over the tail head, and in the sheath of male horses) without generalized obesity and these patients are often more challenging to manage than those with generalized obesity.

Prevalence of laminitis and obesity in horses


Figure 1. Causes of laminitis reported in the 2000 USDA NAHMS study; note that grazing lush pasture was the most common reported cause with a peak incidence in May.
Laminitis is a devastating clinical problem for horses and their owners. In fact, data collected in the 2000 USDA-NAHMS study revealed that laminitis was reported on 13% of horse operations. Further, the leading cause of laminitis was reported to be grazing lush pasture (Figure 1). Similarly, in the United Kingdom more than 8,000 cases of laminitis are estimated to occur annually, representing 7% of the equine population, and more than 60% of cases were classified as pasture-associated disease. In both reports, pasture-associated laminitis had a peak incidence in May, followed by October and November.

Also, as horses have transitioned from beasts of burden to recreational companions, the physical condition of many horses has paralleled that of their human counterparts: they have been overfed and become more sedentary. As a consequence, obesity is becoming a significant problem in the equine species. In a recently studied cohort of horses aged 4-20 years in Virginia, 19% of 300 horses were classified as obese, defined as a body condition score (BCS) of 7.5 or greater on a scale of 1 through 9.

Pathophysiology

The cause of obesity is fairly straightforward: caloric intake exceeding daily caloric requirement. Clearly, there is also a genetic predisposition towards development of obesity that has been referred to as having "thrifty genes". Unfortunately, obesity has a number of metabolic consequences including insulin resistance (IR), hyperglycemia, altered tissue-level cortisol activity, increased leptin concentrations, altered lipid metabolism with hypertriglyceridemia, increased expression of inflammatory cytokines, and hypertension. In horses, the most obvious clinical sign that results from these metabolic alterations is laminitis. EMS appears to have some parallels to the human metabolic syndrome - a syndrome of IR and visceral adiposity (deposition of omental fat) that is recognized to affect an increasing number of middle-aged people. In affected humans, cardiovascular disease, hypertension, dyslipidemias, and type II diabetes (insulin resistant diabetes) are the common sequelae.

In horses, EMS is usually not recognized (or perhaps acknowledged) until insidious-onset laminitis develops in overweight horses that have no obvious risk factors for laminitis (e.g., grain overload, colic or diarrhea with endotoxemia, pleuropneumonia, or retained placenta). Hindsight often reveals that affected horses have had a decrease in exercise program (e.g., the primary rider goes away to college) while nutritional restriction was not implemented. Many horses are initially tested for hypothyroidism and serum thyroxine (T4) concentrations may be near or below the lower end of the reference range in affected equids. However, when the hypothalamic-pituitary-thyroid axis is tested dynamically by administration of thyrotropin-releasing hormone, thyroid gland function has consistently been normal. Similarly, horses older than 15 years of age are commonly suspected of having PPID but overnight dexamethasone suppression test results are normal and hirsutism is not a typical clinical sign. Elevated fasting insulin concentrations (>42 uU/ml or >300 pmol/L) may be found in some, but not all, EMS-affected equids. As an example, in the same cohort of Virginia horses described above, 10% were found to have fasting hyperinsulinemia. Although obese horses were more likely to have hyperinsulinemia than those with a BCS ≤6, not all obese horses had an elevated insulin concentration. However, when dynamic testing of tissue sensitivity to insulin is pursued (several methods are available), IR is found to be a consistent feature of this syndrome.


Figure 2. Andalusian mare with EMS and mild laminitis at initial evaluation (2004, 14-years-old, left picture) with a BCS of 8/9 and weight of 1250 lbs and at reevaluation 2 years later after a 160 pound weight loss (2006, 16-years-old, right picture) to a BCS of 6/9; a glucose tolerance test (0.3 g/kg IV) was performed at both times and revealed greater increases in both glucose (left graph) and insulin (right graph) in 2004 (lines with squares) as compared to 2006 (lines with circles); however, it is important to note that fasting insulin concentrations were not remarkably different at these two times emphasizing the limitation of using fasting insulin concentration alone for documentation of insulin resistance.
What is insulin resistance? Simply stated, IR is the metabolic state in which a greater amount of insulin is required to exert the expected physiological effect of glucose uptake by peripheral tissues. IR is most easily documented by detection of hyperinsulinemia after an overnight fast (or at least 6 hours after a grain meal). Unfortunately, because insulin release is a dynamic physiologic response to feeding, fasting serum insulin concentration is not always elevated in horses with the metabolic syndrome. However, increases in serum glucose and insulin concentrations in response to administration of a bolus of glucose are typically exaggerated in horses with insulin resistance (Figure 2). A relatively simple test for IR is an intravenous glucose tolerance test (IVGTT). In the IVGTT, blood glucose concentration is measured before and for 3-6 hours after administration of an intravenous bolus of glucose (0.1-0.3 g/kg). In the normal state, blood glucose and insulin concentrations should return to baseline within 1 to 2 hours. Glucose intolerance (another name for IR) is present when blood glucose and insulin concentrations remain elevated for more than 3 hours after glucose administration.