Insulin resistance and compensation in Thoroughbred weanlings adapted to high-glycemic meals1

Abstract

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.

Effects of feeding state on glycaemic and insulinaemic responses to a starchy meal in horses: a methodological approach

“…Similar to our findings, higher glucose and insulin responses were reported in aged horses (.20 years) than in young horses (,5 years) after an oral glucose challenge (Ralston et al, 1988;Malinowski et al, 2006). Recent research indicates a negative impact on insulin sensitivity in horses fed high glycaemic meals over a period of months (Hoffman et al, 2003;Treiber et al, 2005). In the present study before the start of experiments, the young horses were mainly on a grass-or hay-based diet with less exposure to starch.…”

“…In most studies, a 10-to 18-h overnight fast is described, and no additional forage was given to the horses during the postprandial blood sampling period (Stull and Rodiek, 1988;Vervuert et al, 2003Vervuert et al, , 2004Vervuert et al, , 2007Vervuert et al, , 2008aVervuert et al, , 2008bVervuert et al, and 2008cJose-Cunilleras et al, 2004;Zeyner et al, 2006). In other studies, ad libitum access to hay was offered the night before and during the blood sampling procedure (Hoffman et al, 2003;Treiber et al, 2005). The data from literature provide evidence that the feeding state before feeding of the test diet might influence the glycaemic and insulinaemic responses.…”

Identificação dos níveis séricos do fator de crescimento tipo insulina 1 em potros com osteocondrose

“…O aumento compensatório da secreção de insulina manteria a homeostase da glicose, mas alteraria a sinalização da insulina em outros sistemas, como no eixo somatotrófico, aumentando o risco de osteocondrose (Ralston 1996, Treiber et al 2005.…”

Development of insulin resistance in horses (Equus caballus): etiologic and molecular aspects

“…Laminitis is a systemic disease and manifests as a noninfectious condition of the foot of the animal. The high carbohydrate diets that may exacerbate insulin resistance (Treiber et al, 2005;Miller and Colagirui, 1994) and predispose humans to type-2 diabetes mellitus (WHO, 1999) and coronary heart disease (Adult Treatment Panel III, 2002) may cause laminitis in equines (Kahn, 1978;Jeffcott and Field, 1985). The Equine Metabolic Syndrome is a predisposition for the development of laminitis and is characterized by obesity, insulin resistance, hypertension and dyslipidemia (Winkelsett and Vervuert, 2008).…”