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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.
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