Insulin resistance and compensation in Thoroughbred weanlings adapted to high-glycemic meals

Insulin resistance has been suggested to increase the risk of certain diseases, including osteochondrosis and laminitis. Our objective was to evaluate the effect of adaptation to high-glycemic meals on glucose-insulin regulation in healthy Thoroughbred weanlings. Twelve Thoroughbred foals were raised on pasture and supplemented twice daily with a feed high in either sugar and starch (SS; 49% nonstructural carbohydrates, 21% NDF, 3% crude fat on a DM basis) or fat and fiber (FF; 12% nonstructural carbohydrates, 44% NDF, 10% crude fat on a DM basis). As weanlings (age 199 ± 5 d; BW 274 ± 5 kg) the subjects underwent a modified frequently sampled i.v. glucose tolerance test. A series of 39 blood samples was collected from -60 to 360 min, with a glucose bolus of 300 mg/kg BW injected at 0 min and an insulin bolus of 1.5 mIU/kg BW at 20 min. All samples were analyzed for glucose and insulin, and basal samples also were analyzed for plasma cortisol, triglyceride, and IGF-I. The minimal model of glucose and insulin dynamics was used to determine insulin sensitivity (SI), glucose effectiveness, acute insulin response to glucose (AIRg), and disposition index (DI). Insulin sensitivity was 37% less (P = 0.007) in weanlings fed SS than in those fed FF; however, DI did not differ (P = 0.65) between diets because AIRg tended to be negatively correlated with SI (r = -0.55; P = 0.067). This finding indicates that the SI decrease was compensated by AIRg in the weanlings adapted to SS. This compensation was further demonstrated by greater insulin concentrations in SS-adapted weanlings compared with FF-adapted weanlings at 11 of 36 sample points (P < 0.055) and greater (P = 0.040) total area under the insulin curve in SS than in FF weanlings. Plasma cortisol and triglycerides did not differ between dietary groups, but IGF-I was greater (P = 0.001) in SS weanlings. Despite appearing healthy, horses adapted to high-glycemic feeds may exhibit changes in altered insulin sensitivity and compensation that increase the risk of diseases involving insulin resistance. These changes seem to be partially amenable to dietary management.