Equine Metabolic Syndrome

Abstract

The term equine metabolic syndrome (EMS) was first introduced to veterinary medicine in 2002 when Johnson1 proposed that obesity, insulin resistance (IR), and laminitis were components of a clinical syndrome recognized in horses and ponies. The study of EMS is therefore in its infancy, so the following consensus statement reflects our current knowledge of this condition. We anticipate that defining features of the EMS phenotype, approaches to diagnostic testing, and management options will be expanded and updated as further research is performed. "EMS" was adopted as the name for this condition because of similarities with the metabolic syndrome (MetS) in humans, which is a collection of risk factors assessed to predict the occurrence of coronary artery disease and type 2 diabetes mellitus in people.2 Despite alternative nomenclature having been proposed previously (eg, peripheral Cushing's syndrome, prelaminitic metabolic syndrome), it was the unanimous decision of the consensus panel to support the use of the term EMS because it has gained wide acceptance and is appropriate when used to define a clinical syndrome unique to equids. The panel proposed that the EMS phenotype for the majority of affected equids should include: Increased adiposity in specific locations (regional adiposity) or generally (obesity). Regional adiposity is characterized by expansion of subcutaneous adipose tissues surrounding the nuchal ligament in the neck (cresty neck), development of fat pads close to the tail head, or fat accumulation behind the shoulder or in the prepuce or mammary gland region. Obesity is observed in the majority of cases, but some affected equids have a leaner overall body condition and regional adiposity, and others are normal in appearance. These different phenotype variations require further study. IR characterized by hyperinsulinemia or abnormal glycemic and insulinemic responses to oral or IV glucose and/or insulin challenges. A predisposition toward laminitis. Clinical or subclinical laminitis that has developed in the absence of recognized causes such as grain overload, colic, colitis, or retained placenta. Additional components of the EMS phenotype that warrant further consideration include: Hypertriglyceridemia or dyslipidemia as a component of EMS in some cases.3–5 Increased very low-density lipoprotein triglyceride concentrations have also been detected in horses with EMS.5 Hyperleptinemia resulting from increased secretion of the hormone leptin by adipocytes in response to IR or a state of leptin resistance.6 Leptin is referred to as a satiety factor because it signals the hypothalamus that a state of energy excess exists within adipose tissues.7 Arterial hypertension4,8 detected in the summer in laminitis-prone ponies,8 which is recognized as a key component of MetS related to IR in humans.9 Altered reproductive cycling in mares. Loss of the seasonal anovulatory period10 and prolongation of the interovulatory period11 have been described in obese insulin-resistant mares. Increased systemic markers of inflammation in association with obesity.12 Contributing factors for obesity should be assessed from the history, including the quantity of feed provided, size and quality of the pasture, and amount of exercise. Horse owners sometimes refer to affected horses and ponies as "easy keepers" or "good doers" because they require a lower plane of nutrition to maintain body weight than other horses. Previous episodes of laminitis may be described in the history. Mild episodes of bilateral laminitis may have been mistakenly attributed to sole bruising, arthritis, or foot soreness after trimming or shoeing. If laminitis episodes have been recognized in the past, it should be noted whether the onset of lameness was associated with changes in the abundance or composition of pasture grass, or alterations in grain feeding. Familial patterns have been recognized for EMS,3 so relevant information about the horse's dam and sire should be collected for future reference. Clinical signs of EMS include regional adiposity, obesity, bilateral lameness attributable to laminitis, and/or evidence of previous laminitis such as divergent growth rings on the hooves. A cresty neck score13 has been developed to assess the expansion of adipose tissues within the neck region and scores range from 0 to 5. Scores ≥3 are often detected in horses or ponies with EMS. The description provided for a score of 3 is "Crest enlarged and thickened, so fat is deposited more heavily in middle of the neck than toward poll and withers, giving a mounded appearance. Crest fills cupped hand and begins losing side-to-side flexibility." Neck circumference can also be measured at the midpoint of the neck with a tape measure. This measurement is taken halfway between the poll and the withers when the neck is in a normal elevated position.5 The neck circumference-to-height at withers ratio was recently used to predict the development of pasture-associate