Also sometimes called Peripheral Cushings, Insulin Resistance or Obesity Dependant Laminitis (ODL).

These names have been given to the metabolic changes that have been identified as a specific medical condition that up until now has just been attributed to animals being overfed and under exercised.

Obesity in humans produces similar changes and has been termed "Metabolic Syndrome" which is why many have adopted the name Equine Metabolic Syndrome for the condition in horses.

Both species typically have high insulin and high blood glucose, but whereas heart disease and hypertension are of most significance in humans, laminitis is by far the most significant condition resulting from it in horses.

Metabolic Syndrome in humans


Increased incidence of obesity in humans in the Western World, particularly the USA (~1/4 of the population fit the clinical picture of metabolic syndrome).

Characterised by:

  • Development of obesity
  • Insulin Resistance
  • Glucose Intolerance
  • Hypertension
  • Activation of inflammatory processes


Combined effects of inappropriate diet, lack of exercise and the development of obesity in genetically susceptible individuals.

Attributed to:

  • Acquisition and persistence of hormonally active fat in susceptible individuals.
  • Fat is no longer thought to be an inert store of energy and produces a number of hormones (adipokines) helping to regulate body shape.
  • Fat stores in different sites produce different adipokines. The most significant ones in humans are the omental adipocytes (in the abdomen).
  • As well as adipokines, omental fat cells also have an enzyme 11 -HSD-1 which converts the inactive cortisone to the active cortisol. Both the cortisol and some of the adipokines inhibit the action of insulin and cause insulin resistance.


I don't know

In those individuals with excess abdominal fat.

Cardiovascular disease and hypertension are common symptoms in humans but not recognised in animals.

Is referred to in humans as Type 11 Diabetes.

Equine Metabolic Syndrome


Occurs in obese horses and ponies, particularly "native" breeds. These breeds seem to be more genetically susceptible and nature would have them store fat when food is plenty in the summer and to use up fat stores in winter when the food is short.

Problem: If we followed this line then the saddle would only fit twice a year!

Characterised by:


Combined effects of inappropriate diet, lack of exercise and the development of obesity in genetically susceptible individuals.

Attributed to:

Acquisition and persistence of hormonally active fat in susceptible individuals. Fat is no longer thought to be an inert store of energy and produces a number of hormones (adipokines) helping to regulate body shape.

We do not know which fat stores produce which adipokines but could be similar to humans.

Not known but likely that the situation in horses is the same as in humans.


By demonstration of insulin resistance.

Not the best way but by far the simplest way is by blood test. High insulin and moderate to high glucose in fasted (no food for 5 hours) horses strongly suggests insulin resistance.

From clinical symptoms, but these are very similar to Cushing's Disease (CD). (CD is rare in horses under 15 years of age.)


Insulin is a hormone produced by the pancreas and is released in response to high blood glucose.

Insulin acts on receptors to stimulate glucose uptake by muscle fat and the liver.

Insulin normally maintains blood glucose within a strict range and is an important regulator of food intake and energy balance by acting on receptors in the brain.

In Primary Diabetes (Type 1) the pancreas is unable to produce sufficient insulin to allow normal uptake of glucose into the cells.

Insulin Resistance

The effectiveness of insulin on its cellular targets is interfered with by glucocorticoids (steroids), free fatty acids and adipokines.

Decreased insulin function will lead to increase in blood glucose and this will stimulate more insulin production by the pancreas, giving high blood insulin as well.

The clinical effects of insulin resistance are due to both insufficient glucose uptake and prolonged exposure of some cells to the high levels of plasma insulin.

Insulin directly increases the sensitivity of tissues to the effects of glucocorticoids.

The horse pancreas is able to maintain this increased secretion of insulin for many years, whereas the human pancreas becomes "exhausted" and is unable to maintain the high insulin production.

Pancreatic B-cell exhaustion following prolonged insulin resistance leads to Type-2 Diabetes in humans.

How is Insulin Resistance Involved in the Development of Laminitis?

We do not know.

Possible factors.

In humans, chronic insulin resistance affects vascular smooth muscle tone and causes hypertension. Hypertension has been shown to occur in chronic founder ponies but we have no evidence that it plays any part in the development of laminitis.

Prolonged high glucose levels change the haemostatic properties of blood vessels, coagulation proteins and platelets, all of which could affect blood perfusion.

It has been demonstrated that the laminal epidermal basal cell attachments are dependant on adequate glucose uptake. For insulin resistance to be a factor, the basal cells would have to significantly depend on insulin-mediated glucose uptake. It is suggested that this is unlikely at this site and it is more likely that glucose uptake is regulated by non-insulin dependant mechanisms and could be affected by other factors present with insulin resistance. ( See Pathogenesis)

How should we manage Insulin Resistance?

Insulin resistance and Type-2 Diabetes are controlled in humans by reducing and changing the diet and by taking exercise.

What do we do with overweight insulin resistant ponies? We restrict their diet, and confine them to small areas, thus reducing their exercise! Can this really be right? I do not think so.

Mikines et al 1988 showed that acute exercise improved insulin sensitivity for up to 48hr. Freestone et al 1992 showed that insulin sensitivity was improved by restricting the diet of ponies but was improved more, and more rapidly, in ponies that were exercised had a restricted diet. Human Type-1 Diabetics have to control their blood glucose with the use of insulin injections. If they take exercise the have to reduce the insulin dose or eat more food, indicating that there is increased uptake of glucose into the tissues.

I believe that we should manage insulin resistance in ponies by restricting their diet, by turning them out with a muzzle rather than confining them to a "bald patch", and also by making sure that they are given regular exercise.

To prevent insulin resistance occurring we should feed only sufficient for the horse's requirements and make sure they are exercised regularly.

P.J.Johnson: The equine metabolic syndrome (peripheral Cushing's syndrome). Vet Clin. N Am: Equine Practice 18 pp271-293 2002

Professor P.J.Johnson - Equine Metabolic Syndrome: Mechanisms of insulin resistance and the role of adipose tissue as an endocrine organ. Proceedings of the Dodson & Horrell International Conference on Feeding Horses. Feb 2005 PP29-39

J.F.Freestone, R.Beadle, K.Shoemaker, R.T.Bessin, K.J.Wolfsheimer and C.Church - Improved insulin sensitivity in hyperinsulinaemic ponies through physical conditioning and controlled feed intake. Equine Vet.Journal 24 pp187-190

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