IN-DEPTH: GERIATRIC MEDICINE/METABOLICS
Table 1. Summary of Findings Related to Obesity, Regional Adiposity, and Endocrine/Metabolic Variables in Published Studies of the Equine Metabolic Syndrome Phenotype
Treiber et al, 20065 Breed(s) Sample size
Obesity (BCS) in EMS
Regional adiposity in EMS
Hyperinsulinemia in EMS
Insulin resistance in EMS
* Frank et al, 20068
Welsh/Dartmoor ponies Six breeds 160 Yes
12 Yes
Yes Yes
Yes (CGIT)
Bailey et al, 20086 Mixed-breed ponies 80
No No
Fasting glucose Not different Triglycerides
NEFAs Not different
Higher in EMS (83.9 vs 66.9 mg/dL)
Higher in EMS (97.2 vs 52.3 mg/dL)
Not different
Higher in EMS (366.5 vs 197.1 mol/L
Yes† (RISQI) Not different
Carter et al, 20097
Yes Yes
Yes (21.6 vs 10.7 mU/L) Yes (50.5 vs 9.1 mU/L) Yes† (69.5 vs 21.5 mU/L) Yes (20.5 vs 8.8 mU/L) Yes (RISQI)
Yes (RISQI) Not different
Higher in EMS† (0.55 vs 0.38 mmol/L 49.0 vs 34.0 mg/dL)
Not evaluated
Higher in EMS (53.0 vs 39.0 mg/dL)
Not evaluated
BCS indicates body condition score; RISQI, reciprocal of the square root of the serum insulin concentration; CGIT, combined glucose-insulin tolerance test; NEFAs, nonesterified fatty acids. *Data obtained from the same population of Welsh and Dartmoor ponies. †Serum insulin and triglyceride concentrations and RISQI differed between ponies with and without a history of laminitis in summer but not in winter.
*
Welsh/Dartmoor ponies 74
pituitary pars intermedia dysfunction) can be re- garded as endocrinopathic in origin. Similarly, pasture-associated laminitis has sometimes been used synonymously with EMS. This report de- scribes current understanding of the clinical fea- tures of EMS as well as underlying pathophysiology. Other papers in this In-Depth series describe meth- ods for diagnosis of EMS and aspects of nutritional and medical management.
2. Defining the EMS Phenotype
Johnson1 recognized that primary features of a laminitis-prone phenotype (ie, obesity, insulin resis- tance) were analogous to those described for the metabolic syndrome (MetS) in humans, which is a constellation of abnormalities, including obesity, dyslipidemia, glucose intolerance, and hypertension associated with increased risk of cardiovascular dis- ease and perhaps also diabetes mellitus.4 The sug- gestion that the underlying pathophysiology of EMS is similar to that of MetS and the increased clinical recognition of “EMS” has spurred a number of ob- servational and experimental studies in the past decade. Data emerging from these studies have provided some insight regarding features of the phe- notype and its pathophysiology. In a published consensus statement from the American College of Veterinary Internal Medicine (ACVIM),2 the EMS phenotype was defined by the following criteria.
(1) Generalized obesity and/or increased adi-
posity in specific locations (regional adiposi- ty): An increase in the amount of fat
298 2013 Vol. 59 AAEP PROCEEDINGS
surrounding the nuchal ligament (“cresty neck”) is a common example of regional adiposity in affected animals but abnormal fat deposits also may be evident close to the tail head, behind the shoulder, or in the prepuce of the mammary gland region. (2) Insulin resistance (IR) characterized by hy- perinsulinemia and/or abnormal glycemic and in- sulinemic responses to oral or intravenous (IV) glucose or insulin challenges. (3) A predisposition toward laminitis that de-
velops in the absence of other recognized causes, such as grain overload, retained placenta, colitis, colic, or pleuropneumonia.
However, descriptions of the metabolic phenotype
of laminitis-prone horses and ponies have varied among published studies (Table 1),5–8 and the fea- tures that define EMS are a subject of ongoing de- bate in the equine veterinary community. What has become increasingly clear is that the relation- ships between the primary phenotypic features and key diagnostic measurements inEMSare complex— its phenotypic manifestation is highly influenced by environment; variation in measurements be- tween individuals caused by breed, age, sex, and other factors make it difficult to establish clear di- agnostic criteria; and not all components of the syn- drome (eg, obesity) may be present in individuals with underlying metabolic derangements. In the following sections, we discuss these key criteria, the current scientific data that support/refute these criteria, and what is known regarding the patho- physiology of EMS.
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