BACKGROUND: After nutrient ingestion there is an early response of glucagon-like peptide 1 (GLP-1) immunoreactivity, although GLP-1 is mainly produced in endocrine cells from the lower gut (ileum and colon/rectum), suggesting that indirect stimulation is important after the ingestion of carbohydrates that are predominantly absorbed from the upper intestine. METHODS: To enable contact of sucrose with lower gut mucosa, sucrose was administered by mouth with and without the simultaneous ingestion of 100 mg of the alpha-glucosidase inhibitor acarbose to six normal healthy volunteers. RESULTS: There was an early increment in GLP-1 15 min after sucrose ingestion. With acarbose, sucrose reached the colon approximately 120 min after ingestion, as indicated by an increment in breath hydrogen exhalation (p < 0.0001), and GLP-1 release was prolonged (p < 0.0001). The sucrose-related increments in glucose, insulin, C-peptide, and gastric inhibitory polypeptide (GIP) and the suppression of glucagon were only marginally affected by acarbose administration. CONCLUSIONS: GLP-1 release appears to be influenced by indirect mechanisms (early response after sucrose) and by direct luminal contact with lower gut mucosal endocrine cells (late response with acarbose).
BACKGROUND: After nutrient ingestion there is an early response of glucagon-like peptide 1 (GLP-1) immunoreactivity, although GLP-1 is mainly produced in endocrine cells from the lower gut (ileum and colon/rectum), suggesting that indirect stimulation is important after the ingestion of carbohydrates that are predominantly absorbed from the upper intestine. METHODS: To enable contact of sucrose with lower gut mucosa, sucrose was administered by mouth with and without the simultaneous ingestion of 100 mg of the alpha-glucosidase inhibitor acarbose to six normal healthy volunteers. RESULTS: There was an early increment in GLP-1 15 min after sucrose ingestion. With acarbose, sucrose reached the colon approximately 120 min after ingestion, as indicated by an increment in breath hydrogen exhalation (p < 0.0001), and GLP-1 release was prolonged (p < 0.0001). The sucrose-related increments in glucose, insulin, C-peptide, and gastric inhibitory polypeptide (GIP) and the suppression of glucagon were only marginally affected by acarbose administration. CONCLUSIONS:GLP-1 release appears to be influenced by indirect mechanisms (early response after sucrose) and by direct luminal contact with lower gut mucosal endocrine cells (late response with acarbose).
Authors: T D Müller; B Finan; S R Bloom; D D'Alessio; D J Drucker; P R Flatt; A Fritsche; F Gribble; H J Grill; J F Habener; J J Holst; W Langhans; J J Meier; M A Nauck; D Perez-Tilve; A Pocai; F Reimann; D A Sandoval; T W Schwartz; R J Seeley; K Stemmer; M Tang-Christensen; S C Woods; R D DiMarchi; M H Tschöp Journal: Mol Metab Date: 2019-09-30 Impact factor: 7.422