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Glucagon-like Peptide 1 (7-36 hide) Secretion in Response to Luminal Sucrose from the Upper and Lower Gut: A Study Using agr-Glucosidase Inhibition (Acarbose) 

Authors: C. Qualmann ab;  M. A. Nauck ab;  J. J. Holst ab;  C. oslashSrskov ab; W. Creutzfeldt ab
Affiliations:   a Division of Gastroenterology and Endocrinology, Dept. of Medicine, Georg-August University, Gottingen, Germany
b Depts. of Medical Anatomy and Physiology, Panum Institute, University of Copenhagen, Copenhagen, Denmark
DOI: 10.3109/00365529509101597
Publication Frequency: 12 issues per year
Published in: journal Scandinavian Journal of Gastroenterology, Volume 30, Issue 9 September 1995 , pages 892 - 896
Formats available: PDF (English)
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Abstract

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 100mg of the agr-glucosidase inhibitor acarbose to six normal healthy volunteers.

Results: There was an early increment in GLP-1 15min after sucrose ingestion. With acarbose, sucrose reached the colon approximately 120min 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).
Keywords: Acarbose; enteroinsular axis; gastric inhibitory polypeptide; glucagon-like peptide 1 (7-36 amide); agr-glucosidase inhibition; incretin hormones; reactive hypoglycemia
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