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

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 weight0.75 per d, or a high-fat diet (FH) fed at 2.10 MJ GE/kg live weight0.75 per d. At the end of the period two acute tests were performed. For acute test 1 the accustomed meal (diets CL, FL and 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 greater than FH greater than FL; P less than 0.05). Plasma insulin concentrations were significantly higher in group CL compared with groups FL and FH (P less than 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 FH than in groups CL and FL (P less than 0.05). There were no differences in plasma insulin concentrations. Plasma glucose (0-300 min) concentrations were significantly higher in groups FL and FH compared with group CL (P less than 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 less than 0.001). Diet FH significantly increased the average GIP content of the small intestine compared with diets CL and FL (P less than 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.