laminitis. Insulin dysregulation is the key feature of the syndrome. It is found in both horses and ponies and has also been recognized in donkeys. 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.
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Equine Metabolic Syndrome

Mar 23, 2020


Adapted from “Overview of Equine Metabolic Syndrome”
By Janice E. Kritchevsky , VMD, MS, DACVIM, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University

Equine metabolic syndrome (EMS) is a characteristic collection of clinical signs and clinicopathologic changes in equids that places them at high risk for developing laminitis. Insulin dysregulation is the key feature of the syndrome. It is found in both horses and ponies and has also been recognized in donkeys. 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.
 
Previously, this cluster of clinical signs in horses was referred to as hypothyroidism, peripheral Cushing disease, prelaminitic syndrome, or Syndrome X. EMS replaces these earlier terms. EMS may be the end result of an inability to properly metabolize dietary carbohydrate, and many horses exhibit exaggerated glucose and insulin responses to an oral hexose load before developing true insulin resistance. Any abnormality in carbohydrate metabolism in horses has been termed insulin dysregulation.

EMS develops:
  • First in horses 5–16 years old, with no recognized sex predilection
  • most commonly in ponies, Saddlebred, Tennessee Walking, Paso Fino, Morgan, Mustang, and Quarter horses
  • Infrequently in 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, both within and between breeds. 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.

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.

Experimentally, high blood insulin levels lead 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.

Horses with EMS respond to high carbohydrate meals with an exaggerated increase in insulin, a higher than expected blood glucose level, and a very slow return of blood glucose concentrations to baseline values. This indicates a resistance to the peripheral effects of insulin (EMS) and/or an inability to metabolize oral carbohydrate normally (insulin dysregulation).

Selecting the proper feed for horses with EMS is key. Pinnacle Low Starch (#319) would be a great choice to begin a feeding horses that exhibit this kind of problem. For more information on what your horse should be eating contact your local Co-op.  
 
 

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