Research Information System
Research Square, vol.0, no.0, pp.1-14, 2023 (Non Peer-Reviewed Journal)
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 junk 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 junk 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.