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Ghrelin, the growth hormone secretagogue receptor ligand, is a key regulator of adiposity and food intake. However, the regulation of ghrelin in response to dietary fat intake remains largely unclear. Furthermore, cephalic elevation of ghrelin may influence fat absorption and postprandial lipaemia. Therefore, the aim of this study was to examine the effect of fat ingestion and vagal stimulation on the regulation of plasma ghrelin.Vagal stimulation was achieved by modified sham feeding (MSF). Eight healthy subjects (four male/four female) consumed a 50 g fat load on two separate occasions. On one occasion, the fat load was preceded by the MSF of a meal for 1 h. Blood, appetite and breath were analysed for 5 h postprandially.A 25% (S.E.M. 3.4) suppression in ghrelin concentration was observed after fat ingestion (P<0.001), without an increase in glucose or insulin. MSF in addition to oral fat enhanced ghrelin suppression further, as well as elevating plasma triacylglycerol (P<0.001) and reducing appetite (P<0.001). The fasting ghrelin concentration was inversely correlated with gastric half-emptying time (P=0.036).We conclude that ghrelin release may be influenced directly by both vagal stimulation and oral fat ingestion.
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Glucagon-like peptide (7-36) amide (GLP-1) is an incretin hormone of the enteroinsular axis released rapidly after meals despite the fact that GLP-1 secreting cells (L-cells) occur predominantly in the distal gut. The importance of these colonic L-cells for postprandial GLP-1 was determined in healthy control subjects and in ileostomy patients with minimal small bowel resection (<5 cm). Subjects were fed a high complex carbohydrate test meal (15.3 g starch) followed by two carbohydrate-free, high fat test meals (25 g and 48.7 g fat respectively). Circulating levels of glucose, insulin, glucagon, glucose insulinotrophic peptide (GIP) and GLP-1 were measured over a 9-h postprandial period. For both subject groups the complex carbohydrate test meal failed to elicit a rise in either GIP or GLP-1. However, both hormones were elevated after the fat load although the GLP-1 concentration was significantly reduced in the ileostomist group when compared with controls (P=0.02). Associated with this reduction in circulating GLP-1 was an elevation in glucagon concentration (P=0.012) and a secondary rise in the plasma glucose concentration (P=0.006). These results suggest that the loss of colonic endocrine tissue is an important determinant in the postprandial GLP-1 concentration. Ileostomists should not be assumed to have normal enteroinsular function as the colon appears to have an important role in postprandial metabolism.
