Insulin resistance in the horse: Definition, Detection, and Dietetics
D. S. Kronfeld*3, K. H. Treiber*, T. M. Hess*, and R. C. Boston†
*Middleburg Agricultural Research and Extension Center, Virginia Polytechnic Institute and State University, Middleburg 20117; and †School of Veterinary Medicine, University of Pennsylvania, Kennett Square 19348
Complete Study: http://jas.fass.org/cgi/reprint/83/13_suppl/E22.pdf
Specific quantitative methods for determining insulin resistance have been applied to obesity, activity/inactivity, reproductive efficiency, and exercise in horses, but only nonspecific indications have implicated insulin resistance as a risk factor or component of equine diseases. Insulin resistance derives from insulin insensitivity at the cell surface, which regulates glucose availability inside the cell, or from insulin ineffectiveness due to disruption of glucose metabolism inside the cell. Interplay of insensitivity and ineffectiveness should be considered in regard to patterns of disease, such as laminitis.
Detection of insulin insensitivity is made weakly on the basis of fasting hyperinsulinemia, more strongly with a statistically validated surrogate, such as the logarithm of the reciprocal of basal insulinemia, or best by a specific quantitative method. Subjects found to be at risk can be managed to improve their insulin sensitivity by dietetics. Claims for dietetic prevention of a disease should be distinguished from claims for avoidance of a dietary risk factor. The evidence required for a claim of prevention is a controlled intervention trial as for a therapeutic drug, according to the U.S. FDA.
Insulin resistance/IR has been implicated in the pathogenesis of equine diseases, such as laminitis, pituitary adenoma, hyperlipidemia, and osteochondritis dessicans. It is affected by fatness/leanness, inactivity/activity, diet, and of avoidance is association revealed by population studies plus causation shown by mechanistic experiments, as formulated in the Surgeon General of the Public Health.
In this view, no appropriate evidence is available for the prevention or treatment of insulin resistance in an equine disease. Evidence is available, however, to justify avoidance of high-glycemic feeds, such as high starch intakes in grains, clover, and alfalfa, and high fructan intakes in grasses, to decrease the risk of acute digestive disturbances associated with rapid fermentation, and chronic metabolic disorders associated with insulin resistance.
During submaximal exercise, high-glycemic meals have been shown to increase glucose utilization immediately. On the other hand, chronic adaptation to feeds that exchange corn oil and fiber sources for sources of sugar and starch confers benefits to athletic performance that may be due to several aspects of fat adaptation, including the regulation of insulin sensitivity, as well as glycolysis and lipid oxidation by signals from insulin receptors.
Information regarding insulin resistance suggests methods for protecting health and promoting horse performance. endotoxin administration. It also influences reproductive efficiency and probably exercise.
The field was initiated by Himsworth (1935), who observed that insulin administration depressed the oral glucose tolerance curve in some diabetic patients (insulin
sensitive), but not others (insulin insensitive). It expanded substantially when IR was found to be a risk factor for several human diseases, for example, coronary
heart disease, hypertension, and polycystic ovarian syndrome, in addition to diabetes mellitus type 2.
A provocative hypothesis is that genetic predisposition to IR is aggravated by a higher-carbohydrate diet in humans. The primary target was the high-carbohydrate diet promoted as heart-protective by public health advocates. The hypothesis resonates in the horse because an increased risk of several digestive and metabolic disorders has been associated with feeding meals of grain and molasses. Thus, the safe use or avoidance of rapidly digested, highcarbohydrate meals, which induce insulin insensitivity , offers management opportunities with regard to avoiding certain diseases and promoting performance.
Insulin resistance alludes to insensitivity at the cell surface and to several disorders inside the insulin-sensitive cells, notably in muscle, adipose tissue, and liver.
An oft-cited definition was proposed by Kahn (1978):
“Insulin resistance [exists] whenever normal concentrations of hormone produce a less than normal biologic response.” He proposed that IR could occur at any of three levels: before the cell receptor, at the cell receptor, and distal to the cell receptor.