The impact of prolonged hyperinsulinaemia on glucose transport in equine skeletal muscle and digital lamellae.
Authors: de Laat M A, Clement C K, Sillence M N, McGowan C M, Pollitt C C, Lacombe V A
Journal: Equine veterinary journal
Summary
# Editorial Summary Rising rates of equine metabolic disease have brought insulin resistance into sharp focus, particularly because of its association with laminitis—a devastating failure of the digital lamellae's weightbearing function. De Laat and colleagues investigated whether prolonged hyperinsulaemia alters glucose transporter (GLUT) trafficking in skeletal muscle and lamellar tissue, hypothesising that dysregulated glucose uptake mechanisms might contribute to laminitis pathogenesis. Using equine models, the researchers examined how sustained elevated insulin levels affect the distribution and function of GLUTs responsible for cellular glucose uptake, comparing changes between metabolically active muscle tissue and the metabolically sensitive lamellar structures. Their findings revealed that chronic hyperinsulaemia significantly impairs normal GLUT trafficking patterns in both tissue types, suggesting that prolonged insulin resistance doesn't simply reflect poor glucose control but actively disrupts the cellular machinery governing glucose entry. For practitioners managing insulin-resistant horses, this work reinforces that metabolic intervention must address the underlying insulin dysregulation itself; it also points toward lamellar tissue as particularly vulnerable to the cellular consequences of insulin resistance, strengthening the rationale for aggressive metabolic management in predisposed animals before clinical laminitis develops.
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Practical Takeaways
- •Recognition and management of insulin resistance is critical to prevent laminitis, as hyperinsulinaemia directly affects glucose transport in tissues vulnerable to laminitis
- •Horses showing signs of metabolic disease require metabolic screening and dietary management to reduce circulating insulin levels and prevent digital lamellae dysfunction
- •Understanding the molecular basis of laminitis development through glucose transporter dysfunction may guide future preventative and therapeutic strategies
Key Findings
- •Prolonged hyperinsulinaemia alters glucose transporter (GLUT) trafficking in equine skeletal muscle and digital lamellae
- •Dysregulation of glucose metabolism through altered GLUT trafficking may contribute to laminitis pathophysiology
- •Insulin resistance is associated with an increased incidence of metabolic disease and laminitis in horses