Other names for this syndromes: Insulin resistance, obesity-associated laminitis, peripheral Cushing's disease, omental Cushing's
Criteria to meet: 1) Abnormal fat deposits (cresty neck, enlarged fat pads); 2) evidence of laminitis; 3) documentation of
Classic Phenotype - middle-aged horses (> 6 yrs), may be obese (easy keepers), cresty neck, abnormal distribution of fat over the neck, rump,
and prepuce and spontaneous, idiopathic laminitis. It is difficult for these horses to lose weight with dietary restriction
and mares do not often breed successfully. Hair coat is NORMAL. Breed predilections include ponies, Morgans, Paso Finos, Norwegian
Fjords, but can occur in any breed.
These horses had previously been considered (inappropriately) to be hypothyroid by most equine clinicians. Experimentally-induced
hypothyroidism does not produce horses with these physical features. Horses with obesity and laminitis often have low circulating thyroid hormone
concentrations, however, thyroid stimulation tests fail to support the diagnosis of hypothyroidism.
The exact pathogenesis is unknown, but diet, genetics, and exercise all likely play a role.
Diet: feeding diets high in non-structural carbohydrates (NSC including starch, fructans) can lead to the development of obesity
and insulin resistance. NSC = nonstructural carbohydrates = starch + water soluble carbohydrates (WSC). Water soluble carbohydrates
= simple sugars + fructan (experimental studies- fructan can cause laminitis). Diets associated with insulin resistance can
include sweet feeds, hay high in NSC, and in grazing.
Genetics: There has been anecdotal reports of certain breeds more likely to develop metabolic syndrome. Recent publication
with Welsh and Dartmoor ponies revealed that pasture-associated laminitis was consistent with a dominant major gene or genes
with reduce penetrance. "Thrifty gene"
Adipocytes: Omental adipocytes are endocrinologically active, and produce several hormones and cytokines. Omental adipocytes
possess the enzyme, 11B-hyroxysteroid dehydrogenase- (11B-HSD-1) that converts circulating inactive cortisone to the physiologically
active glucocorticoid cortisol.
Exercise: exercise will improve insulin sensitivity.
1. Signalment & Phenotype: (middle-aged fat, obese laminitic horse, normal haircoat)
2. Documentation of insulin resistance:
Resting Serum Insulin Concentrations:
Easiest screening test: Measure resting insulin concentrations in horses that have been fasted or only fed grass hay overnight.
Avoid stress (chasing in a field, acute episode of laminitis). Several labs to choose from- but labs will have different normal
values (and different units).
Diagnostic Center for Health and Animal Health at Michigan State University: normal ≤ 300 pmol/l; (or 43 uunits/ml)
University of Tennessee: ≤ 30 uunits/ml
Down side: mild or early IR – will not yet have hyperinsulinemia; also wide references ranges.
Combined Glucose-Insulin Test:
Better assessment of IR; Measure baseline glucose concentrations. Than infusion of 50% dextrose at 150 mg/kg bwt, followed
by infusion of 0.1 units/kg of regular insulin. Blood samples collected for glucose concentrations at 1,5, 25, 35, 45, 60,
75, 90, 105, 120, 135, 150 min post infusion. Insulin resistance defined as blood glucose above resting values for 45 min.
Down side: small chance for hypoglycemia (keep 2 60 ml syringes of 50% dextrose ready- give if blood glucose < 40 mg/dl or
clinical signs of hypoglycemia; stress will affect the values (including pain from laminitis, recommended use a catheter.
Horses should be feed a grass hay overnight, and during the test.