Researchers funded by the Animal Health Foundation (AHF) announced June 15, 2011. that they have made a major breakthrough in understanding how the insulin form of laminitis occurs. Drs. Melody de Laat and Chris Pollitt of the Australian Equine Laminitis Research Unit at the University of Queensland have discovered that receptors designed to receive insulin-like growth factor-1 (IGF-1) are binding to insulin instead in horses with high levels of insulin.

This groundbreaking discovery may enable scientists to develop strategies to try to block IGF-1 receptors from receiving insulin and prevent the disease from occurring.

The receptor also has been shown to be responsible for the metastasis of malignant tumors in humans, and drugs are being developed to block the receptor. These drugs may be of use in trying to treat horses who are prone to laminitis from developing high levels of insulin.

Pollitt and his team, funded by AHF since 1995, previously showed that high insulin is one of the major pathways that cause laminitis, but, to this point, they had not understood how.

The equine foot is very dependent on glucose for metabolism, but it is not dependent on insulin to deliver that glucose. Horses have a large number of IGF-1 receptors in their feet, but no insulin receptors. Pollitt's team now theorizes that these IGF-1 receptors are being stimulated by insulin that mimics IGF-1 and is binding to these receptors.

When this happens, the laminar epithelial cells start to proliferate. Normally these cells in the middle of the foot don't multiply. The cells are made at the coronary band and migrate all the way down to the sole without multiplying.  This type of proliferation causes the laminae to stretch and lengthen and the weight of the horse to ruin the bond between the external hoof wall and the bone. The bone changes position, and laminitis occurs.

"We're starting to understand the pathway of how insulin really causes laminitis," said Dr. Don Walsh, president of the Animal Health Foundation, (ahf-laminitis.org), based in Pacific, Missouri.

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