South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
in taking up and storing fat. Excess fat in liver and muscle tissue has been demonstrated to inhibit
glucose uptake by these tissues. Decreased glucose uptake subsequently leads to increased insulin
release and hyperinsulinemia. With either advancing age or inheritance of “thrifty genes”,
mitochondrial density and function in skeletal muscle is also reduced. Lower mitochondrial
oxidation of fat can also lead to excess fat in skeletal muscle.
Interestingly, it is becoming clear that adipocytes are not simply repositories of stored energy.
Adipocytes also produce hormones (adipokines) that act throughout the body. One of these
hormones is leptin and there is a clear association between obesity and elevated serum leptin
concentrations in horses. Another of these hormones is resistin – it is named for the fact that it
plays a substantial role in IR. It remains to be seen what roles these hormones play in
development of EMS. Of interest, obese horses can either have low (1-5 ng/ml) or high (10-50
ng/ml) plasma leptin concentrations. Horses with high leptin concentrations have a greater insulin
response to glucose administration and it has been speculated that hyperleptinemia could be a
concurrent risk factor for EMS and development of laminitis. Despite the fact that obesity is an
important risk factor for human metabolic syndrome, it has also been recognized that not all obese
people develop the clinical problems clustered under the metabolic syndrome. Adipocytes also
produce a family of adiponectins, peptide hormones that actually enhance insulin action. It is
currently speculated that higher circulating concentrations of these peptides may be a protective
factor against development of the complications of obesity. Clearly, the pathophysiology of IR
with obesity is complex and incompletely understood at this time
Diagnosis: In horses, EMS is usually not recognized (or perhaps acknowledged) until insidiousonset laminitis develops in overweight horses that have no obvious risk factors for laminitis (e.g.,
grain overload, colic or diarrhoea with endotoxaemia, pleuropneumonia, or retained placenta).
Hindsight often reveals that affected horses have had a decrease in exercise (e.g., the primary rider
goes away to college) while the diet was not similarly reduced. In the past, many EMS horses
were initially tested for hypothyroidism and serum thyroxine (T4) concentrations were often found
to be near or below the lower end of the reference range, leading to frequent supplementation with
exogenous thyroid hormone. However, when the hypothalamic-pituitary-thyroid axis has been
tested dynamically by administration of thyrotropin-releasing hormone, thyroid gland function has
consistently been normal. Similarly, horses older than 15 years of age are commonly suspected of
having PPID but overnight dexamethasone suppression test results are normal and hypertrichosis
is not a typical clinical sign.
At present, diagnosis of EMS is based on physical characteristics, specifically obesity and/or
regional fat deposits with or without laminitis. Further support for EMS can be demonstrated by
measurement of insulin concentration. Elevated basal insulin concentrations may be found in
some, but not all, EMS-affected equids. As an example, in the cohort of Virginia horses described
above, 10% were found to have hyperinsulinemia. Although obese horses were more likely to
have hyperinsulinemia than those with a BCS <6, not all obese horses had an elevated insulin
concentration. It has been recommended that horses should be fasted overnight prior to measuring
insulin concentration the following morning, because even hay feeding can cause a mild increase
in insulin in EMS-affected horses. However, if management changes to accomplish fasting (e.g.,
confinement or separation from herd mates) would cause undue stress, horses can be sampled in
the fed state (or while grazing pasture). Realistically, however, detection of hyperinsulinemia in
either the fasted or fed states would be supportive of EMS. Consequently, initial screening can
likely be performed at any time of the day, regardless of feeding state. Again, an elevated insulin
concentration (>200 pmol/L [~30 mU/L]) would support IR. In contrast, a normal fasting insulin
concentration only excluded persistent hyperinsulinemia, not IR. When the fasting insulin
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