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Relationship Between High NSC Diet, Insulin, Proteoglycan, and DSLD in Horses

Relationship Between High NSC Diet, Insulin, Proteoglycan, and DSLD in Horses

The relationship between a high non-structural carbohydrate (NSC) diet, insulin, proteoglycan, and degenerative suspensory ligament desmitis (DSLD) in horses involves interconnected metabolic and structural processes. Below is a concise explanation of how these factors are related, based on available evidence: 

High NSC Diet and Insulin: 

  • A diet high in NSCs (sugars and starches, typically >10-12% NSC) causes rapid spikes in blood glucose, triggering insulin release to regulate glucose uptake.
  • In horses with insulin dysregulation (common in equine metabolic syndrome), high NSC intake leads to hyperinsulinemia (elevated insulin levels) or poor insulin sensitivity, increasing metabolic stress. 

Insulin and Proteoglycan Metabolism: 

  • Chronic hyperinsulinemia may influence connective tissue metabolism by activating pathways like the mitogen-activated protein kinase (MAPK) or increasing expression of bone morphogenetic protein 2 (BMP2), which regulates proteoglycan synthesis. 
  • Proteoglycans are critical components of the extracellular matrix in tendons and ligaments, providing structural support. Abnormal insulin signaling may lead to excessive or dysregulated proteoglycan production. 

Proteoglycan and DSLD: 

  • DSLD, also termed Equine Systemic Proteoglycan Accumulation (ESPA), is characterized by excessive proteoglycan deposition in connective tissues, including suspensory ligaments, tendons, and other structures like the nuchal ligament and blood vessels. 
  • This accumulation disrupts the biomechanical integrity of tissues, leading to weakened ligaments, dropped fetlocks, hyperextension, and progressive lameness. 

High NSC Diet, Insulin, and DSLD: 

  • While DSLD is primarily considered a genetic disorder (with hereditary patterns noted in breeds like Peruvian Pasos), a high NSC diet may act as an environmental trigger or exacerbating factor in predisposed horses.
  • Insulin dysregulation from high NSC intake could amplify systemic inflammation or metabolic stress, potentially worsening proteoglycan dysregulation in DSLD-affected tissues. 
  • The overlap between DSLD and endocrinopathic laminitis (linked to insulin dysregulation) suggests shared pathways, as both involve connective tissue stress, but direct causation between high NSC diets and DSLD remains unproven. 

Summary of Relationships: 

  • High NSC Diet → Insulin: High NSC intake causes insulin spikes, potentially leading to insulin dysregulation or hyperinsulinemia. 
  • Insulin → Proteoglycan: Dysregulated insulin may alter proteoglycan synthesis via pathways like MAPK or BMP2, contributing to abnormal accumulation. 
  • Proteoglycan → DSLD: Excessive proteoglycan deposition in connective tissues is a hallmark of DSLD, weakening ligaments and causing clinical signs. 
  • High NSC Diet ↔ DSLD: High NSC diets may indirectly aggravate DSLD in genetically susceptible horses by exacerbating insulin dysregulation, but DSLD’s primary cause is likely genetic. 

Key Considerations:

  • Evidence on proteoglycan accumulation in DSLD is mixed, with some studies suggesting similar levels in control horses, indicating other factors (e.g., genetic mutations) may drive DSLD. 
  • Managing horses at risk for DSLD or insulin dysregulation involves low-NSC diets (<10% NSC) and exercise to improve insulin sensitivity. 
  • Select low NSC feeds such as Coolstance copra meal, which has low NSC, oil, and digestible fibre

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