Obesity and Laminitis

In obese horses insulin resistance might also contribute to widespread inflammation and, thus, vasoconstriction (narrowing of the blood vessels), which is the case in human metabolic syndrome.
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"Compelling experimental data have been published to suggest that glucose is essential for the health and strength of the equine hoof-lamellar interface," noted Philip Johnson, BVSc(Hons), MS, Dipl. ACVIM, Dipl. ECEIM, MRCVS, professor of veterinary medicine and surgery at the University of Missouri, at the 2006 AAEP Convention. "Hemidesmosomes (HD) represent the important attachment link between keratinocytes (hoof wall cells) and the underlying lamellar basement membrane (attaching the coffin bone to the hoof wall). Keratinocyte glucose starvation (from the aforementioned decreased movement of glucose into the cells) may weaken HD, which leads to separation of the keratinocyte from the basement membrane. Situations associated with cellglucose starvation, such as IR, might increase the risk for laminitis."

He noted that it remains to be seen whether hoof keratinocytes depend (to any extent) on insulin for their glucose supply; this information is currently unknown. In obese horses insulin resistance might also contribute to widespread inflammation and, thus, vasoconstriction (narrowing of the blood vessels), which is the case in human metabolic syndrome, Johnson added.

"By so doing, IR may, in turn, promote the risk of laminitis. The equine hoof-lamellar microvasculature is extremely sensitive to vasoconstrictors (anything that constricts blood vessels)," he explained. Therefore, adipokine-induced vasoconstriction would pose another pathway for causing laminitis in obese horses

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Christy West has a BS in Equine Science from the University of Kentucky, and an MS in Agricultural Journalism from the University of Wisconsin-Madison.

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