Equine metabolic syndrome (EMS)

Annotations:

•  Pathophysiology of EMS compared to other species   Horses can remain hyperinsulinaemic for years without developing diabetes mellitus You can detect hypernsulinaemia with normal or high-normal glucose concs in horses Do not develop amylin witin the pancreas and progress to diabetes mellitus (while cats and humans do) Diabetes mellitus is rarely seen in horses, and when it is, it is associated with PPID or old age   

1. 1. Adiposity
   1. Physiological for energy storage, but this is too much
      1. Adipokine and adipocytokine production occurs
         1. Chronic low grade inflammation
         2. Adiponectin is an adipokine which is significantly lower compared to controls with higher risk of laminitis
2. 2. Insulin resistance
   1. Caused by:
      1. Accumulation of intracellular lipids (lipotoxicity) in skeletal muscle, liver and pancreas
      2. Down-regulation of insulin signalling pathways by adipokines
   2. 3 stages of IR
3. 3. Laminitis
   1. Occurs in 7 steps:
      1. 1. Hyperinsulinaemia
      2. 2. Endothelial cell dysfunction
         1. Inhibition of NO release by endothelium
         2. Endothelin-1 synthesis and sympathetic nervous activation
      3. 3. Digital vasoconstriction
      4. 4. Impaired glucose uptake from lamellar cells
      5. 7. Pro-inflammatory/pro-oxidative state in lamellar tissue
      6. 5. Altered fusion and mitosis
      7. 6. Activation of matrix metallopreinase

1. Definition
   1. Collection of risk factors which predispose laminitis
      1. Obesity
      2. Insulin Resistance
      3. Dyslipidaemia (HyperTAGaemia)
      4. Hypertension
      5. Altered reproductive cycling
      6. Increased systemic markers of inflammation
2. History
   1. Feed quality/quantity
   2. Exercise
   3. History of laminitis
      1. Look for divergent growth rings on hoof
   4. Season (lush green pastures!)

1. Signalment
   1. 5-15yo (younger horses)

      Annotations:

      • Compare this with PPID - older horses!
   2. Ponies, minis, coldbloods and arabs
   3. Seasonal
      1. Lush green pastures (see note)

         Annotations:

         • During sunshine periods sugars are produced in excess in the grasses These are converted into storage carbohydrates (fructans and starches)   
2. Clinical signs
   1. Obesity
      1. BCS 3-5
      2. Enlarged/thickened crest
      3. Regional adiposity may make BCS difficult
      4. HOWEVER
         1. Lean horses may be seen with EMS
            1. § 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1) is an enzyme which increases local production of cortisol in adipose tissue, this promotes insulin resistance
            2. § Pancreatic disease can result in reduced insulin production and T2DM
   2. Lameness
      1. Remember, owners only recognise EMS after lameness has developed
         1. This is late in the disease's course