Peripheral Cushing’s syndrome (PCS) is a recently named problem seen in middle-aged horses and ponies with obesity-associated laminitis. These horses tend to accumulate fat in the crest of the neck, over the rump, and in the sheath of males. It was first proposed that classic Cushing’s disease–a pituitary gland disorder that leads to excessive cortisol levels in the blood–was causing the obesity-associated laminitis. (Cortisol is primarily produced by the adrenal gland; some of its effects include conversion of amino acids to glucose in the liver, elevation of blood sugar levels, and promotion of glycogen storage in the liver.)

A significant, sustained rise in the level of cortisol circulating in the blood can result in clinical signs of classic Cushing’s disease, such as a long, curly hair coat and laminitis. However, when tested for classic Cushing’s disease using the overnight dexamethasone suppression test (DST), these overweight, laminitic horses/ponies tested normally, i.e., had normal pituitary gland function.

In “Thyroid Function in Horses with Peripheral Cushing’s Syndrome,” Emily Graves, VMD, of Michigan State University, discussed what researchers have discovered about this disease. In a recent study, researchers at Michigan State evaluated thyroid gland function in horses with PCS to see if thyroid function was normal. They confirmed their hypothesis that the thyroid gland functions normally in PCS-affected horses. Graves said their findings helped to rule out hypothyroidism as a risk factor for development of obesity-associated laminitis.

In addition, preliminary data indicate that oxoreductase activity of 11-beta hydroxysteroid dehydrogenase (HSD) is increased. This enzyme converts inactive cortisone into active cortisol in the peripheral tissues throughout the body. This mimics a human disorder called central obesity or metabolic syndrome, in which elevated HSD action is the cause. The human disorder is serving as a model for further characterization of PCS in horses and ponies