The Effect of Insulin Loaded Nanoparticles on Immuno-reactivity of Beta Cells in Rats with Diabetes Type 1

Abstract

The basic criteria of type 1 diabetes (T1D) are autoimmune destruction of beta cells that eventually leads to a full loss of insulin secretion capability, which is a crucial stage in the disease's pathophysiology. In recent investigations, it was shown that pancreatic tissues from long-term T1D patients included insulin-producing beta cells. These findings suggested the presence of working beta cells that had evaded apoptosis by lowering gene expression. The development of diabetic liver damage has been linked to oxidative stress, the formation of reactive oxygen species (ROS), and diabetes infections linked to beta-cell dysfunction. Other diabetes-related effects include immune-histochemical evaluation of the pancreas in male Wistar rats following oral treatment of insulin-loaded nanoparticles (INS) containing carboxymethyl chitosan nanoparticles (CMCNPs) and gold nanoparticles (AuNPs) independently. Because of their inhibitory and protective impact, beta cells' immunological reactivity was dramatically boosted as compared to the diabetic group, and a reduction in pancreatic inflammation was noted. In conclusion, promising effects of insulin-loaded carboxymethyl chitosan NPs (INS-CMCNPs) and insulin-loaded gold NPs (INS-AuNPs) in controlling and promoting organ functions when compared to subcutaneous insulin were observed. This may provide new evidence for the reversibility of beta-cell dysfunction and insulin insufficiency with precise glycaemic control.