Prolonged and enhanced secretion of glucagon-like peptide 1 (7-36 amide) after oral sucrose due to alpha-glucosidase inhibition (acarbose) in Type 2 diabetic patients

Diabet Med. 1998 Jun;15(6):485-91. doi: 10.1002/(SICI)1096-9136(199806)15:6<485::AID-DIA610>3.0.CO;2-Y.

Abstract

GLP-1, an incretin hormone of the enteroinsular axis with insulinotropic and glucagonostatic activity, is secreted after nutrient ingestion. GLP-1 is mainly produced by intestinal L-cells in the lower gastrointestinal tract (GIT); simple carbohydrates are absorbed in the upper GIT and alpha-glucosidase inhibition leads to augmented and prolonged GLP-1 release in normal subjects. In a cross-over study, 100 mg acarbose or placebo was administered simultaneously with 100 g sucrose to 11 hyperglycaemic Type 2 diabetic patients poorly controlled with diet and sulphonylureas. Plasma levels of GLP-1, insulin, C-peptide, glugacon, GIP, glucose and H2-exhalation were measured over 6 h. Differences in the integrated responses over the observation period were evaluated by repeated measurement analysis of variance with fasting values used as covariates. With acarbose, sucrose reached the colon 60-90 min after ingestion as indicated by a significant increment in breath hydrogen exhalation (p = 0.005). After an early GLP-1 increment 15 min after sucrose under both conditions, GLP-1 release was prolonged in the acarbose group (p = 0.001; significant from 210 to 360 min.). Initially (0-150 min), glucose (p = 0.001), insulin (p = 0.001), and GIP (p < 0.001) were suppressed by acarbose, whereas later there were no significant differences. Glucagon levels were higher with acarbose in the last 3 h of the 6 h observation period (p = 0.02). We conclude that in hyperglycaemic Type 2 diabetic patients, ingestion of acarbose with a sucrose load leads to elevated and prolonged GLP-1 release.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acarbose
  • Administration, Oral
  • Aged
  • Blood Glucose / metabolism
  • C-Peptide / metabolism
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Diabetes Mellitus, Type 2 / physiopathology
  • Enzyme Inhibitors / therapeutic use*
  • Female
  • Gastric Inhibitory Polypeptide / blood
  • Gastrointestinal Hormones / metabolism*
  • Glucagon
  • Glucagon-Like Peptide 1
  • Glucagon-Like Peptides
  • Glycoside Hydrolase Inhibitors*
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Insulin / blood
  • Male
  • Middle Aged
  • Peptide Fragments / metabolism*
  • Sucrose / pharmacology*
  • Time Factors
  • Trisaccharides / therapeutic use

Substances

  • Blood Glucose
  • C-Peptide
  • Enzyme Inhibitors
  • Gastrointestinal Hormones
  • Glycoside Hydrolase Inhibitors
  • Hypoglycemic Agents
  • Insulin
  • Peptide Fragments
  • Trisaccharides
  • glucagon-like peptide 1 (7-36)amide
  • Sucrose
  • Gastric Inhibitory Polypeptide
  • Glucagon-Like Peptides
  • Glucagon-Like Peptide 1
  • Glucagon
  • Acarbose