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Novartis Institute for Biomedical Research, LSB 3517, Summit, New Jersey 07901
The incretin glucagon-like
peptide-1 (GLP-1)-(7---36) amide is an important factor in prandial
glucose homeostasis. Findings that GLP-1 is rapidly inactivated led to
the hypothesis that the target of GLP-1 is close to the site of
release. To investigate whether the target tissue is located in the
hepatoportal system, we administered GLP-1 with glucose into the portal
vein of rats and compared this with peripheral GLP-1 administration
(jugular vein) and studied the effects of blockers of the nervous
system. Portal GLP-1 augmented the insulin response to a portal glucose bolus by 81% (P < 0.01) and markedly improved the
glucose disposal rate (P < 0.05). Peripheral
administration of GLP-1 produced a similar augmentation of the insulin
response (88%) and of the glucose disposal rate. However, only the
effect of portal GLP-1 on insulin secretion was blocked by the
ganglionic blocker chlorisondamine. The data suggest that prandial
-cell stimulation by GLP-1 is evoked via a neural reflex triggered
in the hepatoportal system. Because absorbed nutrients and GLP-1 first
appear in the portal system, this mechanism may constitute a major
pathway of GLP-1 action during meals.
glucagon-like peptide-1; incretin; autonomic nervous system
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