Glucose homeostasis and the enteroinsular axis in the horse: a possible role in equine metabolic syndrome.
Authors: de Graaf-Roelfsema Ellen
Journal: Veterinary journal (London, England : 1997)
Summary
# Editorial Summary: Glucose Homeostasis and Equine Metabolic Syndrome Hyperinsulinaemia in horses with equine metabolic syndrome (EMS) has traditionally been viewed as a consequence of insulin resistance, yet emerging evidence suggests this relationship is bidirectional—elevated insulin itself actively drives both insulin resistance and obesity, potentially acting as a primary pathogenic driver rather than merely a secondary effect. De Graaf-Roelfsema's 2014 review synthesises current understanding of glucose and insulin metabolism in horses by examining the enteroinsular axis (the coordinated intestinal and pancreatic responses governing postprandial glucose handling), hepatic and peripheral tissue glucose uptake, and the physiological mechanisms underlying normal versus dysregulated insulin secretion. Key insights centre on how dietary composition influences incretin hormone release and subsequent postprandial insulin dynamics—factors that differ meaningfully between equine and human physiology—and how disrupted glucose sensing at the intestinal level can perpetuate the hyperinsulinaemic state characteristic of EMS. Understanding these mechanisms shifts clinical focus beyond simply identifying insulin resistance toward recognising how primary enteroinsular dysfunction and sustained hyperinsulinaemia may initiate the cascade leading to metabolic syndrome. For practitioners managing EMS cases, this framework emphasises the importance of dietary intervention targeting postprandial glycaemic control and suggests that early modulation of insulin secretion, rather than waiting for overt insulin resistance to develop, may represent a more preventative approach to disease management.
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Practical Takeaways
- •Managing EMS in horses requires attention to diet composition and meal structure to modulate postprandial insulin responses, not just caloric restriction
- •Hyperinsulinaemia should be monitored and controlled as both a consequence and driver of metabolic dysfunction, as it perpetuates insulin resistance independent of initial causation
- •Understanding how different tissues handle glucose helps explain why some horses remain insulin resistant despite weight loss, guiding more targeted nutritional and management strategies
Key Findings
- •Hyperinsulinaemia in equine metabolic syndrome can both result from and independently induce insulin resistance and obesity
- •The enteroinsular axis and oral glucose uptake mechanisms play a key role in postprandial insulin responses in horses
- •Diet composition significantly influences incretin hormone secretion and subsequent insulin responses in equine glucose homeostasis
- •Hepatic, muscular, and adipose tissue glucose handling differs between healthy horses and those with disrupted glucose homeostasis