Equine Metabolic Syndrome (EMS) and Insulin Dysregulation

Olde Towne Equine
24 hours ago
2 min read

2024 Recommendations for Diagnosis and Management

Prepared by the 2024 EMS/ID Working Group.

The Equine Endocrinology Group (EEG) provides expert, opinion-based advice to help equine practitioners diagnose and manage endocrine disorders in horses. These guidelines are updated biennially and can be found on the EEG website.

Key Definitions

Equine Metabolic Syndrome (EMS)

EMS is a collection of metabolic and clinical features consistently including insulin dysregulation (ID), which increases the risk of laminitis in horses and ponies. Other variable factors can include:

Regional or generalized obesity
Altered adipokine and postprandial incretin concentrations
Hypertriglyceridemia
Hypertension

An asinine metabolic syndrome has also been identified, with reported reference intervals for insulin concentrations in donkeys.

Insulin Dysregulation (ID)

ID is a disturbance in the relationship between plasma or serum insulin and glucose. It encompasses any combination of:

Resting hyperinsulinemia
Post-prandial or post-challenge hyperinsulinemia
Peripheral or hepatic insulin resistance

Hyperinsulinemia occurs due to excessive insulin secretion from pancreatic beta cells and potentially reduced hepatic clearance of circulating insulin. Diets rich in non-structural carbohydrates (NSC) and incretins (like GIP and GLP-1) are primary stimulators of pancreatic beta cells. Insulin resistance is the inadequate response of insulin-sensitive tissues to insulin.

Hyperinsulinemia-Associated Laminitis (HAL)

HAL is the most prevalent form of laminitis in the general horse and pony population (over 90% of cases), replacing older terms like "pasture-associated laminitis" and "endocrinopathic laminitis." It can develop subtly but often becomes a chronic condition with repeated episodes of mild to severe lameness. This type of laminitis begins with stretching and damage to the digital lamellae, induced by episodes of hyperinsulinemia that may initially go undetected before progressing to lameness. The pathophysiology and histological changes of HAL differ from sepsis-associated laminitis and supporting-limb laminitis. The exact mechanism of HAL is not fully understood, but it seems to involve inappropriate stimulation of insulin-like growth factor-1 receptors (IGF-1R) on lamellar epidermal cells.

Non-Structural Carbohydrates (NSC)

NSCs are dietary components that are the main drivers of insulin secretion. The NSC content in a diet is calculated by adding water-soluble carbohydrates and starch. Older subtraction-based equations are no longer recommended as they include non-fiber carbohydrates (e.g., gums, mucilages, galactans, beta-glucans, neutral detergent soluble cell wall components) that do not impact insulin responses.