05/29/2026
Endocrine-Associated Laminitis
Brian S. Burks, DVM
Diplomate of the American Board of Veterinary Practitioners®
394 Fox Road
Apollo, PA 15613
(724) 727-3481
www.foxrunequine.com
Laminitis occurs when the laminae (leaves) that suspend the third phalanx within the hoof capsule become damaged and inflamed. Given enough damage, they separate, allowing the coffin bone to rotate or sink.
Laminitis is not only a local disease, it is also systemic. About 12% of laminitis cases are caused by colic, diarrhea, retained placenta, or carbohydrate overload. The remaining cases are related to diet, obesity, and/or endocrine disorders- equine metabolic syndrome and pituitary pars intermedia dysfunction (PPID)/equine Cushing’s disease.
Equine metabolic syndrome (EMS) typically causes horses to become obese, with regional adiposity and a cresty neck. They are predisposed to weight gain and refractory to weight loss. Not all EMS horses are obese; some high-risk breeds are thin, and weight loss is not always enough to prevent endocrine disease.
In the United States, 51% of mature light-breed horses are obese. Genetics contribute to body condition and altered endocrine function.
Adipocyte hypertrophy, inflammation and increased CCL2 (cytokine) expression are features of obese adipose tissue in horses but fibrosis and altered adipose tissue expression of insulin-signaling genes are not consistent features. Visceral and retroperitoneal adipose tissue of horses with obesity and EMS is markedly dysfunctional with a hypertrophic-inflammatory phenotype.
Evidence of increased cortisol levels over a prolonged period does exist; there is an abnormal fat pad distribution, elevated circulating insulin levels, glucose intolerance, laminitis, hyperlipemia with hepatic lipidosis, and infertility.
Laminitis is common in these horses due to circulating HSD (11-hydroxysteroid dehydrogenase), leading to elevated endogenous cortisol levels. Other risk factors for laminitis are lacking in these horses. The laminitis may be chronic and low grade, but acute exacerbations can occur. Corticosteroids lead to hyperinsulinemia, which has been shown to cause laminitis. Glucocorticoids enhance the vasoconstrictive effects of epinephrine, norepinephrine, and serotonin. Obese horses have altered blood flow due to endothelial dysfunction from insulin insensitivity and increased vasospasticity. There is also a hypercoagulable state similar to atherosclerosis in humans.
At very high concentrations, insulin can bind to insulin-like growth factor-1 (IGF-1) receptors in the hoof lamellae. This stimulates abnormal cellular proliferation and stretching of lamellar epithelial cells, weakening attachment between the epidermal and dermal lamellae, resulting in lamellar elongation, weakening, and rotation and/or sinking of the distal phalanx.
The nutrition and body condition of a pregnant mare could be another contributing factor to a foal’s endocrine state later in life.
Excess insulin changes glucose handling and intracellular signaling in lamellar cells leading to oxidative stress, cytoskeletal disruption, impaired adhesion molecules, and extracellular matrix remodeling. These changes weaken the basement membrane and lamellar attachments.
Intestinal health may also play a role in that the microbiome of EMS horses is less diverse, similar to humans with metabolic syndrome. Human MS has been linked to loss of intestinal barrier function, increased intestinal permeability or leaky gut syndrome, which adds to systemic inflammation. This likely occurs in horses as well.
Endocrine-disrupting chemicals (EDCs) are also associated with EMS, with reports that they alter gene expression and affect metabolism. Many EDCs persist in fat for prolonged periods.
Insulin-related laminitis occurs mainly in obese horses/easy keepers, horses with insulin dysregulation, grazing on high NSC pasture. This may be triggered by spring grass, grain overload, and stress, which increases insulin resistance.
Dysfunction of the pituitary pars intermedia, usually in older horses, also causes laminitis. That portion of the pituitary hypertrophies, leading to excessive production of pituitary hormones, particularly adrenocorticotropin hormone (ACTH), which in turn amplifies cortisol (the stress hormone) secretion from the adrenal glands. Horses with PPID are hirsute, with long, shaggy coats that do not shed out well, and grow in faster in the autumn. They have abnormal fat distribution and undergo muscle wasting. They drink and urinate excessively and have recurrent infections, such as sinusitis, hoof abscesses, and poor wound healing. Affected horses may be infertile. Many also experience hyperinsulinemia, amplifying the risk of laminitis.
Insulin dysregulation is a consequence of obesity and is also found in many PPID horses, leading to laminitis. Dietary glucose absorbed into the bloodstream stimulates the pancreas to secrete insulin. With ID, cells do not respond to insulin signals to take glucose into muscle, liver, and fat cells. The pancreas then secretes increasing amounts of insulin in an attempt to increase glucose uptake. Normally, the liver clears most insulin, but horses with obesity or ID do not clear insulin as well.
Intestinal changes also contribute to hyperinsulinemia. There are specialized endocrine cells throughout the intestinal tract, along the mucosal surface, and their interaction with the microbiota increases secretion of incretin (stimulating a decrease in blood glucose levels) hormones such as glucagonlike peptides (GLP1 and 2) in response to high nonstructural carbohydrate (NSC) meals, like grain. GLPs are implicated in inducing more pronounced and undesirable insulin responses.
Insulin alters the signaling within the lamellar epithelial cells, causing them to change shape and stretch due to disruption of the cell cytoskeleton.
Endocrine-associated laminitis often begins with a long subclinical phase that causes chronic changes to the hoof capsule. The horse will develop divergent hoof rings that are wider at the heel than the toe that can go all the way down the hoof capsule, indicating that although the horse may not have clinical signs of laminitis, it has been present for at least one year. Others have more obvious signs, including flaring or distortion of the dorsal hoof wall, a flat or convex sole, and widening of the white line region. The horse may develop overt lameness without warning.
This differs from other forms of acute and chronic laminitis related to systemic inflammatory response syndrome (SIRS) that develops from colitis, endotoxemia, placentitis, or carbohydrate (grain) overload. In these cases, inflammatory cells infiltrate the laminae and the basement membrane that soon degenerates and the lamellae fail. This does not occur with endocrine induced laminitis, which is more nebulous.
Knowing that many cases of laminitis are attributable to endocrine disease, steps can be taken for prevention and treatment before lameness is severe. Growth rings in the hoof capsule can be present for many months without lameness, giving the opportunity to control insulin dysfunction and laminar stretching and failure with painful laminitis.
Controlling obesity is paramount to controlling insulin dysfunction and endocrinopathic laminitis. Refrain from overfeeding your horse, and restrict or eliminate pasture turnout during periods of high sugar accumulation in grass. Your veterinarian can help tailor a dietary program that provides sufficient and safe levels of nutrients compatible with your horse’s needs. Implement lifestyle changes that include not only dietary controls but also regular exercise for your horse.
Fox Run Equine Center
www.foxrunequine.com
(724) 727-3481
