The effect of energy source and feeding level on the hormones of the entero-insular axis and plasma glucose in the growing pig

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Abstract
The aim of the experiment was to test the theory that accustoming pigs to a high-fat diet causes exaggerated gastric inhibitory polypeptide (GIP) secretion in response to a high-fat meal, and to determine whether hypersecretion of GIP could be related to an increase in the GIP content of the small intestine. Twenty-four pigs were fed one of three dietary regimens for 11 weeks: a high-carbohydrate diet (CL), or a high-fat diet (FL), both fed at 1.46 MJ gross energy (GE)/kg live weight0.75per d, or a high-fat diet (FH) fed at 2.10 MJ GE/kg live weight0.75per d. At the end of the period two acute tests were performed. For acute test 1 the accustomed meal (diets CLFLand FH) and for acute test 2 a standard high-fat meal (diet FL) were given; blood samples were taken during the next 5 h and analysed for GIP, insulin and glucose. Integrated increases in hormone and glucose levels were compared by analysis of variance (0–300 min). In acute test 1 there were significantly different plasma GIP concentrations between groups (CL> FH> FL;P< 0.05). Plasma insulin concentrations were significantly higher in group CLcompared with groups FLand FH(P< 0.002). There were no differences in glucose levels. In acute test 2 integrated increases in plasma GIP (0–300 min) concentrations were not significantly different; however, GIP (0–45 min) concentrations were significantly higher in group FHthan in groups CLand FL(P< 0.05). There were no differences in plasma insulin concentrations. Plasma glucose (0–300 min) concentrations were significantly higher in groups FLand FHcompared with group CL(P< 0.05). The GIP content of tissue samples taken at the end of the experiment from the duodenum, jejunum, upper and lower ileum decreased significantly in a proximal to distal direction (P< 0.001). Diet FHsignificantly increased the average GIP content of the small intestine compared with diets CLand FL(P< 0.05). It is concluded that fat meal-stimulated GIP secretion was enhanced by increased feeding level during a pre-treatment phase, possibly due to an increase in GIP synthesis in the small intestine. The high-fat diet caused glucose intolerance after a high-fat meal. This may be due in part to the action of dietary fat on glucose transport and metabolism.