Maternal Obesity Effect on Offspring Pancreatic Endocrine Cells: Investigation of the Cell Transdifferentiation

Abstract

Abstract Type 2 Diabetes (T2D) is a disease characterized by impaired functioning of pancreatic beta cells. In the later stages of the disease, beta cell dysfunction is defined as a decrease in functional cell count. Our hypothesis was that obesity-induced hyperglycemia of the mother could lead to dedifferentiation and/or transdifferentiation in their offspring's pancreatic beta cells. In our study, the mother Wistar rats whose obesity was brought on by the human-liked processed food which is called cafeteria diet (CAF), and their offspring were breastfed throughout the lactation phase and then given standard rat chow. Pancreatic tissues of both mother and offspring were obtained to elucidate the transformation profile with gene expression analysis, RT-qPCR. It was revealed that functional beta cell marker gene expressions decreased while progenitor marker gene expressions increased in the CAF group. We also discovered that dedifferentiation was partially presented at the protein level in the pancreas tissues of the CAF mother and offspring groups after analyzing glucagon and insulin protein expressions. Our findings suggest that processed food-induced maternal obesity and consequently T2D may have an impact on the dedifferentiation of pancreatic beta cells in offspring and may be a predisposing effect for diabetes.