| Autor: |
WØJDEMANN, M., WETTERGREN, A., HARTMANN, B., HOLST, J. J. |
| Předmět: |
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| Zdroj: |
Scandinavian Journal of Gastroenterology; 8/20/98, Vol. 33 Issue 8, p828-832, 5p, 1 Chart, 2 Graphs |
| Abstrakt: |
Background: Glucagon-like peptide-2 is formed from proglucagon in the intestinal L-cells and is secreted postprandially in parallel with the insulinotropic hormone GLP-1 (glucagon-like peptide-1), which in addition acts to inhibit gastric motility (enterogastrone effect) by inhibiting central parasympathetic outflow. GLP-2 has no effect on the endocrine pancreas. We here tested the hypothesis that GLP-2 acts as an enterogastrone. Methods: Fourteen anesthetized pigs with their splanchnic nerves cut were subjected to insulin hypoglycemia, and force transducers were sutured to the antrum to record motility. GLP-2 was infused intravenously in doses from 1 to 6 pmol/kg/min after the onset of antral motility in response to hypoglycemia. Results: Insulin hypoglycemia invariably and greatly increased the frequency and amplitude of antral phasic contractions. Infusions of GLP-2 dose dependently (1-6 pmol/kg/min) inhibited antral motility. At 2 pmol/kg/min, resulting in plasma GLP-2 concentrations of 102.5 ± 19 pmol/l (normal postprandial range, 30-82 pmol/l), the motility index was inhibited by 91% ± 14%. Conclusions: Both of the intestinal glucagon-like peptides may operate as hormonal transmitters of the ileal brake effect. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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