THE EFFECT OF ENERGY-SOURCE AND FEEDING LEVEL ON THE HORMONES OF THE ENTEROINSULAR 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 (C(L)), or a high-fat diet (F(L)), both fed at 1.46 MJ gross energy (GE)/kg live weight 0.75 per d, or a high-fat diet (F(H)) 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 C(L), F(L) and F(H)) and for acute test 2 a standard high-fat meal (diet F(L)) 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 (C(L) and F(H) and F(L); P <0.05). Plasma insulin concentrations were significantly higher in group C(L) compared with groups F(L) and F(H) (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 F(H) than in groups C(L) and F(L) (P <0.05). There were no differences in plasma insulin concentrations. Plasma glucose (0-300 min) concentrations were significantly higher in groups F(L) and F(H) compared with group C(L) (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 F(H) significantly increased the average GIP content of the small intestine compared with diets C(L) and F(L) (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.