Effect of glukagon-like peptide-1 analog Liraglutidee on neural tube development in chick embryo model

Incretin-based glucagon-like peptide-1 (GLP-1) receptor agonists are used in the treatment of type 2 diabetes and obesity. From the presence of beta in the pancreas, a blood-dependent mechanism for the purpose of insulin develops, inhibits glucagon secretion, and protects the beta cellfrom apoptosis. While reducing food intake, it delays gastric reduction, causes weight loss and provides protection on the nervous system. The aim of the thesis study is to scan different doses of Liraglutid on the neural tube in a chick embryo model, which is similar to first month development in mammals. 100 eggs of 61 ± 5 gr, specific pathogen-free 0 day white fertilized chicken eggs obtained from İzmir Bornova Veterinary Control and Research Institute were used. Our thesis study presented was done jointly with our department and Afyonkarahisar Health Sciences University, Faculty of Medicine, Department of Anatomy. Incubation of 28 hours was maintained at a constant temperature of 37.5 ± 0.5°C, humidity in the range of 60 – 68% and automatically rotated at an angle of 45° every 2 hours. They were divided into 4 groups of 25 eggs each. Liraglutid was administered subblastodermically with a Hamilton micro-injector in 3 different doses. At the end of the 48th hour, all eggs were opened and embryos were removed and evaluated macroscopically, microscopically and histopathologically. In the study, 1.5 micrograms for low doses, 7.5 micrograms for medium doses, and 15 micrograms for high doses of Liraglutid injected eggs were used. The control group was studied as sham. Staining was done with Hematoxylin-Eosin and May-Grünland-Giemsa solution. In group 1, after the injection of Liraglutid 30 microgram/kg/1.5 microgram/per egg, the neural tube was closed in 20 embryos (80%), the neural tube was open in 1 embryo (4%), 1 embryo had developmental delay (4%), 1 no disc was formed in the embryo (4%) and there was an opening error in 2 embryos (8%), the fore-aft measurement was 660.37 ± 20.98 µm, the somite number was between 11 - 12 stages according to the Hamburger Hamilton scale, In group 2, after the injection of Liraglutid 150 micrograms/kg/7.5 micrograms/per egg, the neural tube was closed in 19 embryos (76%), the neural tube was open in 3 embryos (12%), there was a developmental delay in 1 embryo (4%), 1 no disc was formed in the embryo (4%) and there was an opening error in one embryo (4%), the fore-aft measurement was 660.20 ± 30.39 µm, the number of somites was between 11 - 12 stages according to the Hamburger Hamilton scale, In group 3, after the injection of 300 microgram/kg/15 microgram/ peregg Liraglutid, the neural tube was closed in 19 embryos (76%), the neural tube was open in 3 embryos (12%), there was developmental delay in 1 embryo (4%), and the disc in 1 embryo. (4%) and one embryo had a defect in opening (4%). The fore-aft measurement was 631.62 ± 31.05 µm, the number of somites was between 11 - 12 stages according to the Hamburger-Hamilton scale, In group 4, sham, no procedure was performed and the neural tube was closed in 21 embryos (84%), the neural tube was open in 1 embryo (4%), there was developmental delay in 1 embryo (4%), and in 2 embryos no disc was formed (8%) fore-aft measurement was 670.50 ± 30.14 µm, somite number was 16.27 ± 1.24, according to Hamburger-Hamilton scale, in the 11-12 stage range. In the examination of neural tube patency, somite counts, and Hamburger-Hamilton stages, it was determined that the dose-related difference between the control and experimental groups was not statistically significant (p>0.05). While the mean fore-and-aft lengths were similar in the control group (670.50 µm) and low dose (660.37 µm) and medium dose (660.20 µm) groups, it decreased to 631.62 µm in the high dose group and in the high dose group and other groups. The difference between the two was found to be statistically significant (P<0.05). As a result, there was no significant relationship between the doses of Liraglutid and neural tube patency and somite counts, but differences were found between fore-aft measurements. The Liraglutid teratogenic mechanism is not clear; therefore, more research needs to be done.