Ucp2 gen analysis in pancreas and hippocampus of obese rat model

Obesity is a risk factor associated with many complex diseases such as cardiovascular diseases, type 2 diabetes. It is important to elucidate the molecular mechanisms that cause obesity. Pancreas, which is effective in energy metabolism by affecting blood glucose level, is an important in diabetes and obesity. UCP2 in the pancreas regulates the release of insulin and glucagon. UCP2 in the hippocampus affects learning processes by playing a role in neuronal regeneration. In this study, possible relationships between learning and Ucp2 gene expression in hippocampus and pancreas were analyzed in obese rats. An experimental obesity model was established in Wistar albino adult male rats. In the experiments, 16 animals, 8 obese and 8 controls were used. Hippocampal and pancreatic tissues were dissected. Ucp2 gene expression level was determined in tissues using RT-quantitative-PCR method. Qiagen data analysis was used for the comparison of gene expression levels. The evaluation of the learning data was done by the student-T test. The level of Ucp2 gene expression in the hippocampus was increased in the obese group compared to the control group and statistically significant at the border (p=0,05), not different in the pancreas (p=0,94). When the learning performance were compared, it was found that lower in the obeses than the controls (p=0.001). Obesity was found to reduce learning performance. The increased expression of the Ucp2 gene in the hippocampus was interpreted as a defense of cells for neuronal survival in obesity. Our results will contribute to the researches to be done in this regard.