RESUMEN
Background: glucagons - like peptide-] [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 intracerebral ventricular injection ofGLP-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 3 7 C. The effect ofGLP-1 on Synaptosoms was tested by adding 50 pL qj"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: CLP-I decreased levels of serotonin [5-HT] by 20% [P<0. 05] after 15 minutes of incubation with combined hypothalamus and brain stem Synaptosoms. 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. Gamma-Aminobutyric acid [GABA] and its amino acid precursor glutamic acid [Glu] were both quantities at the same conditions as above, but an 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