The Link Between Insulin Resistance And Laminitis

There is a well-established link between insulin resistance and laminitis (de Laat et al., 2010). However, the mechanism behind this link may not be as well understood.

Insulin is a hormone that regulates glucose uptake from the blood into various cells such as muscle, liver, or fat cells. In horses with a normal metabolic function, when blood glucose levels rise after a meal, the pancreas releases insulin, which moves glucose from the blood into key cells for energy or storage as glycogen. This brings blood glucose levels back to baseline and the release of insulin is reduced.

In horses with insulin resistance, the cells that uptake glucose lose their sensitivity to insulin, meaning glucose is not effectively moved into the cells and blood glucose levels remain high. As a result, the pancreas continues to release insulin, leading to high levels of circulating insulin and glucose. This also leads to cells not receiving the energy (glucose) required for normal functioning.

In addition to this, the insulin dependant cells in the hoof that attach the hoof wall to the pedal bone (keratinocytes) have a reduced uptake of glucose due to the reduced sensitivity to insulin. Glucose deprivation has been shown in-vitro to result in separation of equine hoof-to-bone connective tissue, as the hoof wall lacks the energy required for structure and growth (Pass et al., 1998). This reflects the hoof wall separation and pedal bone rotation that characterises laminitis.

Management of Insulin Resistance

When managing a horse with insulin resistance, it is important to reduce peaks in blood glucose and insulin. This involves using feed and forage that is low in starch and sugar. Keeping meal sizes small by splitting the daily ration across multiple feeds also reduces glucose peaks. For obese horses with insulin resistance, it is important to reduce calorie intake by feeding balancers instead of a traditional mix or cube. It is also important to manage conserved forage and pasture intake, as forage makes up the majority of the horse’s diet, so will have the largest contribution in terms of energy intake. Suggestions to safely reduce calorie intake from forage include, but are not limited to, soaking hay, using slow feeders, feeding a mature stemmy hay with a lower digestible energy level, and restricting grazing where required.

It is important to note that not all horses with insulin resistance are overweight. Maintaining body condition through quality fibre and oil, whilst keeping starch and sugar intake low is recommended for insulin resistant horses that lack condition. For this we recommend Re-Leve® Mix, a high energy, cereal free mix.

In addition to managing starch and sugar intake, omega 3 fatty acid supplementation has been shown to improve markers of insulin sensitivity in insulin resistant horses (Hess et al., 2013). Insulin plays a key role in regulating inflammation, and so increasing the intake of anti-inflammatory omega-3 fatty acids helps to regulate this function. Supplementing with anti-inflammatory omega 3 fatty acids is also recommended for horses recovering from laminitis, due to the potential to reduce inflammation in the hoof wall. Fish oil is a more readily available source of omega 3’s to the horse than linseed or vegetable oil is and is therefore more effective. The omega 3 fatty acid (ALA) in vegetable oil must be converted in the horse's body into the form that can be used, which is an inefficient process. The omega 3 fatty acids (EPA and DHA) in fish oil are already in the form the horse can use, so does not need to be converted, making it more bioavailable. For a highly bioavailable marine derived omega 3 fatty acid supplement, we recommend KER EO.3™.

de Laat, M.D., McGowan, C.M., Sillence, M.N. and Pollitt, C.C., 2010. Equine laminitis: induced by 48 h hyperinsulinaemia in Standardbred horses. Equine veterinary journal, 42(2), pp.129-135.

Gauff, F., Patan‐Zugaj, B. and Licka, T.F., 2013. Hyperinsulinaemia increases vascular resistance and endothelin‐1 expression in the equine digit. Equine veterinary journal, 45(5), pp.613-618.

Hess, T.M., Rexford, J., Hansen, D.K., Ahrens, N.S., Harris, M., Engle, T., Ross, T. and Allen, K.G., 2013. Effects of Ω-3 (n-3) fatty acid supplementation on insulin sensitivity in horses. Journal of Equine Veterinary Science, 33(6), pp.446-453.

Pass, M.A., Pollitt, S. and Pollitt, C.C., 1998. Decreased glucose metabolism causes separation of hoof lamellae in vitro: a trigger for laminitis?. Equine veterinary journal, 30(S26), pp.133-138.

Peroni, J.F., Moore, J.N., Noschka, E., Grafton, M.E., Aceves-Avila, M., Lewis, S.J. and Robertson, T.P., 2006. Predisposition for venoconstriction in the equine laminar dermis: implications in equine laminitis. Journal of Applied Physiology, 100(3), pp.759-763.

Treiber, K.H., Kronfeld, D.S. and Geor, R.J., 2006. Insulin resistance in equids: possible role in laminitis. The Journal of nutrition, 136(7), pp.2094S-2098S.