Insulin resistance (IR) in horses describes a condition in which the body fails to properly respond to the hormone insulin.

Impaired insulin response is the main feature of Equine Metabolic Syndrome (EMS). Horses with EMS do not metabolize sugars properly and have difficulty losing weight.

This form of metabolic dysfunction is associated with some telltale signs in horses including generalized obesity or regional adiposity, including along the neck (“cresty neck”). Other signs include subclinical or overt laminitis, increased appetite, reproductive issues and poor performance.

EMS and insulin resistance are treated with dietary intervention, exercise, and sometimes require medication. If your horse shows signs of being insulin resistant, consult with your veterinarian to obtain a diagnosis and work with a nutritionist to formulate an appropriate diet.

Overview of Insulin Resistance

Insulin resistance is diagnosed in horses with an elevated blood insulin level (hyperinsulinemia). Insulin is a hormone produced by the pancreas in response to high blood sugar levels (hyperglycemia). [1]

When a horse consumes carbohydrate-containing foods, the stomach breaks the food into components including glucose (sugar) so it can be absorbed into the blood. High levels of glucose in the blood subsequently stimulate the pancreas to release insulin.

Insulin is essential for regulating blood sugar metabolism because it facilitates glucose uptake from the bloodstream into certain tissues, including muscle, liver and adipose tissue (fat).

In healthy tissues, insulin binds to its receptor on the cell membrane and signals cells to take in glucose. In insulin resistant tissues, signaling is less effective after insulin binds to the receptor.

Failure to respond to insulin means that glucose is not adequately transported from the bloodstream into cells, resulting in high blood glucose levels. The body overcompensates by producing more insulin to promote the uptake of glucose. [1] This causes elevated insulin levels which can be picked up in a diagnostic test.

Hyperinsulinemia is an integral part of Equine Metabolic Syndrome (EMS) and the direct cause of damage to the laminae of the hoof in horses with laminitis.

The vast majority of horses with metabolic syndrome are able to maintain blood glucose in a normal zone when fed the correct diet and, if needed, medication. Animals that are sound and can be exercised do best. [2][3] If persistent glucose elevations do develop (diabetes), the only consequence that has been appreciated to date is weight loss. [4]

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8 Signs of Insulin Resistance in Horses

Not all horses with IR will show the same clinical signs or symptoms and some horses may give no outward signs that they are insulin resistant.

However, common indications of impaired insulin sensitivity include:

1) Obesity

While some IR horses are not overweight, many are overweight or obese and have a body condition score ranging from six to nine on a nine-point scale. [5][6]

While it is widely believed obesity predisposes to metabolic syndrome in people, the same is not the case with horses. Lindase et al induced obesity by feeding fat in a cohort of horses that already had high insulin. The diet resulted in a 10% increase in weight but no change in insulin. [7]

Bamford et al similarly induced obesity with a high fat diet and in one group also fed a high carbohydrate meal daily. Again, the weight gain failed to induce insulin resistance. In fact, the addition of a high carbohydrate meal improved insulin sensitivity. [8]

Obese horses may have difficulty losing weight because of leptin resistance. Leptin is a hormone produced by adipose (fat) cells and acts on the brain to control appetite and hunger. Leptin increases as fat mass increases and reduces appetite by acting on the hypothalamus. In other species, leptin resistance is a known contributing factor to insulin resistance and obesity. [9]

Although leptin resistance has not been directly demonstrated in horses, leptin and insulin levels are higher in obese horses compared to those with optimal body condition. [10][11]

2) Laminitis

Elevated insulin levels in metabolic syndrome are associated with the development of endocrinopathic laminitis in horses and ponies. [1] An abnormal insulin level may increase the risk of laminitis by altering the function of the epidermal laminar cells of the hooves.

Laminitis is a painful condition that involves damage to the hoof laminae, the internal structures that attach the wall of the hoof to the coffin bone. Despite the “itis” in its name, endocrinopathic laminitis does not involve inflammation as a cause.

Laminitis can result in lameness and downward rotation of the coffin bone (founder). In very severe cases, laminitis can cause separation between the wall of the hoof and the coffin bone. The prognosis for recovery is poor in horses with advanced cases except with intensive nursing for a prolonged period of time.

Although the exact mechanisms of how hyperinsulinemia promotes laminitis are still being researched, vasoconstriction, and endothelial damage are proposed disease pathways.

Additionally, horses with IR and EMS may be more sensitive to steroid administration (e.g. joint injections, steroids given for skin or respiratory allergies) and could be inadvertently pushed into a laminitic episode in situations of otherwise routine steroid use. [12]

3) Excessive Drinking and Urinating

Healthy, non-working, non-breeding adult horses typically drink 60 mL/kg of body weight of water each day. [13] For a 500 kg (1100 lb) horse, this is approximately 30 litres per day.

Horses with high glucose levels urinate more frequently to eliminate some of the excess glucose via urine. This increases thirst and leads to increased water intake. [14]

However, horses with metabolic syndrome rarely become diabetic with high blood sugar. If excessive drinking and urinating are seen, it is likely because the horse also has PPID. [15]

4) Loss of Muscle Mass

Horses with pituitary pars intermedia dysfunction (PPID) have age-related degeneration of dopaminergic neurons in the hypothalamus of the brain. These neurons control a specific region of the pituitary gland in the brain (the intermediate lobe).

Horses with PPID can also have concurrent insulin resistance. PPID is a distinct disease that results from excessively high levels of adrenocorticotropic hormone (ACTH) that increases cortisol production which can promote muscle loss. [16]

In other species, inflammation related to insulin resistance can cause muscle atrophy. This is due to increased protein breakdown and reduced protein synthesis in skeletal muscle. [17]

However, in horses markers of inflammation in skeletal muscle are lower in obese horses and lowest of all in obese horses with high insulin. [18] Therefore, it is unclear whether inflammation plays a role in muscle atrophy in horses.

5) Abnormal Fat Deposits

Obese horses that are insulin resistant often develop excess fat deposits due to increased conversion of sugar into fat. This is particularly true in donkeys and mules but also found in ponies, minis and horses. Insulin resistance in adipose tissue also limits the ability to release fat from these storage sites.

Fat deposits are commonly seen on the neck (cresty neck), over the ribs and topline, above the eyes, and at the base of the tail. Fat deposition may occur in the sheath of geldings and around the mammary gland of mares.

6) Excessive Hunger

Horses that are obese and insulin resistant often have a higher level of leptin circulating in their blood. [19][20] Leptin is a hormone released by fat cells that helps to inhibit hunger.

Research in other species shows an association between insulin resistance and leptin resistance. When the hypothalamus in the brain becomes resistant to the effect of leptin, satiety signalling fails to occur. [21] Leptin resistance may lead to increased appetite in obese horses, although further research is needed to confirm the relationships between insulin, appetite and leptin levels in horses.

7) Inflammation

In humans, there is a clear connection between obesity, infiltration of fat deposits by immune cells and subsequent release of inflammatory cytokines. [22] However, wh