Insulin resistance refers to the inability of insulin to exert its physiologic effect of facilitating the movement of glucose from the blood into insulin-sensitive tissues, such as muscle and adipose (fat) tissue. Because glucose isn’t cleared from the blood it stays elevated, and stimulates the pancreas to release more insulin, resulting in hyperglycemia (high blood glucose) and hyperinsulinemia (high blood insulin), respectively.

Insulin resistance is difficult to diagnose in a clinical setting, therefore the scientific community is using the term insulin dysregulation (ID) to describe abnormal glucose and insulin dynamics. ID describes an excessive amount of insulin released with carbohydrate consumption or administration, basal hyperinsulinemia and/or true tissue insulin resistance. ID is a concern as it is associated with an increased risk of laminitis, and is a component of Equine Metabolic Syndrome.

Insulin resistance can develop over time, when horses consume regular meals that are high in soluble carbohydrates. It is believed that the repeated rises in blood glucose following high sugar meals and the resultant peaks in insulin down regulate the tissue’s responses to insulin. Many horses that develop insulin resistance are overweight, and research has shown that adipose (fat) tissue produces inflammatory proteins that can also affect insulin signaling. Horses that have Cushing’s Disease (PPID) may also develop insulin resistance. This is because Cushing’s affects horses that have increased cortisol production – a hormone that essentially counteracts the effects of insulin in part by promoting glucose production and release by the liver. Cortisol also promotes visceral fat development, which can further impair insulin function.

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