Graduate Student University of Guelph brampton, Ontario, Canada
Abstract:
Background: Hyperglycemia is associated with mortality in horses. A key system in controlling glycemia and pancreatic function is the enteroinsular axis which consists of the incretin hormones glucagon-like peptide-1 (GLP-1), glucagon-like peptide-1 (GLP-2), and glucose-dependent insulinotropic polypeptide (GIP). Information on incretins in healthy and sick horses is lacking.
Objective: Investigate the enteroinsular axis in healthy horses and horses with colitis and to determine their association with mortality. Animals: 29 healthy horses and 91 horses with colitis (66 survivors, 24 non survivors).
Methods: Prospective case control study. Plasma insulin, glucose, GLP-1, and GIP concentrations were determined on admission. Data were analyzed by non-parametric methods and univariate analysis.
Results: Glucose was numerically, but not statistically, higher in non-surviving (n=23; 7.5 mg/dl, 4.8–9.5) than surviving (n=63; 5.9 mg/dl, 5.3–7) horses with colitis (P=0.05). GIP was significantly lower in horses with colitis (n=93, median: 42 ng/ml, range: 31–90) than healthy (n=29; 105 ng/ml, 50–165] horses (P=0.01). GIP was lower in non-surviving (n=24; 36 ng/ml, 17 – 53) than surviving (n=66; 49 ng/ml, 33–97) horses with colitis (P=0.01). Horses with colitis and low GIP were more likely to die or be euthanized (OR=1.02, 95%CI=1.002–1.036). GLP-1 was significantly higher in horses with colitis (n=18, median: 48 ng/ml, range: 34–69) than healthy (n=4; 22 ng/ml, 18–29] horses (P=0.01).
Conclusions: Dysregulation of the enteroinsular axis occurred in horses with colitis. Hyperglycemia in non-surviving horses with colitis can be explained, at least in part, by impaired intestinal production of GIP.
