Abstract
Background: Glucagons - like peptide-1 (7-36) amide (GLP-1) is the main product of the
glucagon gene expression in intestinal L cells. GLP-1 is released from the intestine into the
circulation in response to the ingestion of food and is the most potent stimulator of glucose-induced
insulin secretion. GLP-1 receptors have also been detected in discrete areas of rat brain and
intracerebro ventricular injection of GLP-1 has been shown to inhibit feeding in fasted rats.
Methods and Materials: This study is an in vitro study. Used rats are male and their weight is 200
to 220 grams and each group has 7 rats. In this study HPLC techniques were employed to evaluate
the effects of GLP-1 on monoamine metabolism in rat brain as a neuropeptide.
Synaptosoms were prepared from homogenates of combined hypothalamus and brain stem from
rats in each group. The synaptosomal pellets incubated for 15 minutes in ashaker bath at 37 C. The
effect of GLP-1 on synaptosoms was tested by adding 50 μL of GLP-1 5x10 –7 M to the incubation
medium. For this group a control group was prepared by adding normal saline instead of GLP-1.
The data were analyzed by T- test.
Results: GLP-1 decreased levels of serotonin (5-HT) by 20% (P<0.05) after 15 minutes of
incubation with combined hypothalamus and brain stem synaptosomes. Level of 5-
hydroxyindolacetic acid (5-HIAA), the principal metabolite of 5-HT, and tryptophan, the amino
acid precursor of 5-HT decreased by 21% and 37 %( P<0.05) respectively. γ-Aminobutyric acid
(GABA) and its amino acid precursor glutamic acid (Glu) were both quantities at the same
conditions as above , but a operculum derivatization HPLC technique was used. The increase levels
of GABA (14%) and Glu(6%) by GLP-1 was not significant .
Conclusions: The results suggest that decreased synaptosomal levels of 5-HT and 5-HIAA caused
by GLP-1 are due to diminished availability of tryptophan by the neuropeptide.
glucagon gene expression in intestinal L cells. GLP-1 is released from the intestine into the
circulation in response to the ingestion of food and is the most potent stimulator of glucose-induced
insulin secretion. GLP-1 receptors have also been detected in discrete areas of rat brain and
intracerebro ventricular injection of GLP-1 has been shown to inhibit feeding in fasted rats.
Methods and Materials: This study is an in vitro study. Used rats are male and their weight is 200
to 220 grams and each group has 7 rats. In this study HPLC techniques were employed to evaluate
the effects of GLP-1 on monoamine metabolism in rat brain as a neuropeptide.
Synaptosoms were prepared from homogenates of combined hypothalamus and brain stem from
rats in each group. The synaptosomal pellets incubated for 15 minutes in ashaker bath at 37 C. The
effect of GLP-1 on synaptosoms was tested by adding 50 μL of GLP-1 5x10 –7 M to the incubation
medium. For this group a control group was prepared by adding normal saline instead of GLP-1.
The data were analyzed by T- test.
Results: GLP-1 decreased levels of serotonin (5-HT) by 20% (P<0.05) after 15 minutes of
incubation with combined hypothalamus and brain stem synaptosomes. Level of 5-
hydroxyindolacetic acid (5-HIAA), the principal metabolite of 5-HT, and tryptophan, the amino
acid precursor of 5-HT decreased by 21% and 37 %( P<0.05) respectively. γ-Aminobutyric acid
(GABA) and its amino acid precursor glutamic acid (Glu) were both quantities at the same
conditions as above , but a operculum derivatization HPLC technique was used. The increase levels
of GABA (14%) and Glu(6%) by GLP-1 was not significant .
Conclusions: The results suggest that decreased synaptosomal levels of 5-HT and 5-HIAA caused
by GLP-1 are due to diminished availability of tryptophan by the neuropeptide.
Keywords
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Copyright
© 2004, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.