There is a long-recognized syndrome is middle-aged horses characterized by founder (laminitis) and obesity. The characteristic appearance is an overweight, “easy-keeper” horse with a cresty neck and abnormal distribution of fat over the neck, rump, and prepuce/udder. It is difficult for these horses to lose weight with dietary restriction and mares do not often breed successfully. These horses have previously been misclassified as suffering from poor thyroid function, however, removal of the thyroid gland does not produce horses with these physical features. Thyroid stimulation tests fail to support the diagnosis of hypothyroidism, and it is clear that this combination of laminitis and obesity are not manifestations of insufficient thyroid hormone production. Instead, these horses appear to have a disorder resulting in inappropriate production of stress hormone (cortisol) in regional fat depots. Humans are affected by a similar condition termed “omental Cushing’s syndrome”, which produces fat deposition around their abdomen (central obesity). The proposed term for the condition in horses is peripheral Cushing’s or obesity-associated laminitis syndrome. The primary defect is abnormal enzyme activity (11 beta-hydroxysteriod dehydrogenase) resulting in increased cellular cortisol activity (local cortisol excess) and insensitivity of tissues to insulin. The excessive fat depots become a novel source of cortisol production.
Diagnostic testing to confirm peripheral Cushing’s in horses includes determination of serum glucose and insulin concentrations. Moderate elevations in glucose and insulin, and abnormal glucose tolerance are characteristic of peripheral Cushing’s syndrome and classic Cushing’s syndrome (pituitary adenoma). Horses with peripheral Cushing’s syndrome will not develop a long hair coat like horses with classic Cushing’s syndrome. Screening tests for hypothyroidism will be misleading.
There is no specific treatment for obesity-associated laminitis syndrome in horses, however dietary and management changes will produce improvement in clinical signs. Exercise (as permitted by laminitis) will improve glucose tolerance and insulin function. Dietary supplementation with chromium (5 to 10 mg/day) will improve peripheral insulin function and glucose tolerance. Serum glucose and insulin concentrations are reduced, often to normal values, weeks to months after initiation of exercise and dietary chromium supplementation.