Oertzenweg 19 b
+49 30 838 62299
Diabetes mellitus type 2 is a worldwide problem in human medicine as is the equine equivalent “Equine Metabolic Syndrome” (EMS). In humans, an inverse relationship between serum magnesium content and the incidence of diabetes mellitus type II has been shown. Humans with peripheral insulin resistance often show cellular magnesium deficits and multiple studies have demonstrated the beneficial effect of dietary magnesium supplementation on insulin sensitivity. One study has evaluated the effects of magnesium supplementation on insulin sensitivity in laminitic horses and could not find differences. In this previous study, a different magnesium formulation (magnesium oxide) and dosage had been used. The purpose of this study was to evaluate the effects of an oral supplementation with magnesium aspartate hydrochloride in horses with Equine Metabolic Syndrome. This study was performed on five horses (four mares and one gelding) of different breeds, aged seven to 26 years with Equine Metabolic Syndrome based on the results of a CGIT (Combined Glucose Insulin Tolerance Test). In these horses body weight, Body Condition Score (BCS) and Cresty Neck Score (CNS) were assessed. The following blood parameters were measured in the serum: magnesium (Mg2+), ACTH, fructosamine, reciprocal inverse square of insulin (RISQI) and modified insulin to glucose ratio (MIRG). Gamma-glutamyltransferase (GGT) and triglyzerides (TG) were measured in EDTA blood samples. All horses were supplemented with 30 mg/kg BW magnesium as magnesium aspartate hydrochloride for a time period of three month. Afterwards all blood parameters and the CGIT were repeated. A Wilcoxon signed rank test was used for non-normally distributed data. Statistical significance was set at 95%. All horses had increased BCS and CNS (BCS 8 (7-8), CNS 4 (3-4)). The magnesium content in the serum, ACTH, GGT, TG and MIRG before supplementation were within the reference ranges in all horses. The fructosamine content was increased in horses one, four and five. RISQI was decreased in horse five. During the magnesium supplementation, no adverse effects were observed. There were no significant changes in body weight, BCS and CNS. There were also no significant changes regarding serum magnesium concentration, ACTH, RISQI and MIRG or GGT and TG. There was a tendency for decreased fructosamine concentration, which was also not statistically significant. In three of five horses the CGIT after magnesium supplementation was negative. These horses reached their glucose baseline levels after at least 45 minutes, while insulin (baseline and after 45 minutes) was within the reference ranges. The remaining two horses did not show significant differences compared to the beginning of the trial. It is concluded that the supplementation of magnesium aspartate hydrochloride in horses with Equine Metabolic Syndrome can have positive effects on the insulin sensitivity. Further examinations with more horses are necessary.