According to the National Diabetes Fact Sheet 2011, more than 1 million persons in North America have type 1 diabetes (T1D), which is typically brought on by the autoimmune destruction of insulin-producing pancreatic islets. The key to treating T1D is to replace lost beta cells or insulin produced by those beta cells. T1D is frequently treated with insulin. Potential dangers during a lifetime of insulin therapy include sporadic post-injection hypoglycemia and the difficulties related to long-term insulin delivery. Islet transplantation is an experimental treatment for T1D that has the potential to prolong insulin independence, however many trials have shown that it cannot sustain normoglycemia for longer than five years. In order for the new insulin-producing cells to replace the lost beta cells due to autoimmune damage, tremendous work has been put into researching beta cell regeneration during the past 20 years. Beta cell regeneration may hold promise for the treatment of type 1 diabetes in the future by utilising advancements in the fields of protein sciences and regenerative medicine. It is generally acknowledged that while the size of an islet rises with age, the overall number of islets remains constant across a lifetime. Additionally, pancreatic beta cells with a longer lifespan do not usually proliferate. Numerous preclinical investigations, however, showed that some beta cells might restore the ability to multiply with the right stimulus. Beta cell proliferation is a dynamic process, although its intrinsic routes have not yet been fully elucidated. For instance, the gene expression profile of pancreatic beta cells descended from the same ancestor did not alter. Only a small subset of specialised beta cells will regain the ability to proliferate under specific circumstances, according to a recent discovery. However, the bulk of beta cells in islets are replication-resistant and do not respond to mitogenic activation. To encourage beta cell regeneration, two classes of transcriptional factors or hormones have been utilised. Deeply influencing elements for pancreatic beta cell development and differentiation are included in the first group. These substances include pancreatic duodenal homeobox-1 (Pdx1), neurogenin 3 (Ngn3), cyclin D1/D2, cyclindependent kinase 4 (CDK4), glucagon-like peptide-1 (GLP-1), and cyclin D1/D2. The chemical connections between these components were not well appreciated, though. In preclinical investigations, it was found that a number of variables, including CDK4, GLP-1, and Ngn3, could effectively enhance the bulk of pancreatic beta cells. Other mitogenic substances like vascular endothelial growth factor and hepatocyte growth factor are included in the second category (HGF). The beta cell mass in T1D rats was similarly shown to be preserved by these factors, but they were not present in the intrinsic pathways controlling the growth and proliferation of pancreatic beta cells. Therefore, these substances appeared to work mostly in combination with the natural mechanism of beta cell regeneration in a synergistic or additive manner rather than exclusively on pancreatic beta cells. To conclude, new approaches to treating T1D will be developed as our understanding of the mechanisms behind beta cell proliferation grows. The two potential candidates on the horizon appear to be stem cell therapy and betatrophin. Although its mechanism of action is uncertain and additional preclinical proof is required, betatrophin, a star molecule, is paving the way for the first clinical trials in beta cell regeneration because of its ability to work specifically and effectively on pancreatic beta cells. However, stem cell therapy, which is still under preclinical testing, has encountered more real-world difficulties. However, stem cell therapy has proven its potential in numerous reports as a potent immunosuppressant and trophic mediator, which may offer helpful insight into the start of T1D and may prove to be an invaluable assistance in the treatment of the disease.