Biomedical research in the modern era excels at developing cures for illnesses with relatively straightforward causes and well-understood hereditary risk factors. Unfortunately, type 1 diabetes (T1D) has a highly complicated genetic profile, with several genes contributing to disease risk in relatively minor and poorly understood ways. Additionally, there are no appropriate animal models of human illness. Thus, despite hundreds of millions of dollars spent on research on Diabetes Stem Cell Therapy in India, no treatment for T1D has been identified.
A Novel Disease Model
Scientists are undertaking an ambitious, long-term, and high-risk experiment to develop the first animal model for type 1 diabetes. Engineered mice will enable researchers to have a better understanding of the condition and improve the likelihood of generating viable Diabetes Stem Cell Therapy India treatments.
The Conception
Recent developments in stem cell biology have paved the path for novel approaches to investigating type 1 diabetes. Specifically, it is now feasible to reprogram a T1D patient’s (or any other person’s) skin cell into a cell that closely mimics an embryonic stem cell. These new stem cells, dubbed induced pluripotent stem cells (iPS cells), are capable of developing into every type of cell found in the human body. Additionally, because iPS cells are genetically similar to the original patient, they include all of the mutations associated with T1D. This approach is capable of producing an almost infinite number of sick cells.
A Collaborative Organization
The scientist has created an inter-institutional team of specialists in Diabetes Stem Cell Treatment India with a track record of effective collaboration to develop this model, ensuring its success. Medical School, Children’s Hospital, and the Immune Disease Institute is all part of the team.
Constructing Beta Cells
Additionally, Scientists and researchers are researching how Diabetes Stem Cell Treatment India might be used to treat diabetes. The objective is to generate glucose-sensing, insulin-producing beta cells, which are damaged in type I and type II diabetes, respectively. The Scientist is addressing the issue in four distinct ways.
Cells that are dividing
Our team improved the efficiency of the procedure of generating generic pancreatic endocrine cells from embryonic stem cells. It is feasible to grow cells at a sufficiently high size to conduct lengthy studies and be therapeutically effective using a novel bioreactor.
With this in place, researchers are concentrating their efforts on the final stage of the process—converting pancreatic endocrine cells to beta cells. This final stage of maturation has occurred in the live mouse but has not yet occurred in the laboratory environment. Once the procedure is manage, patients will receive the appropriate amount and type of cells.
Differentiation Directed
A second strategy is to convert other pancreatic cell types into beta cells. Douglas Melton, Ph.D., co-director of SCIENTIST, demonstrate that this could be accomplish by converting pancreatic acinar (digestive) cells in a live animal into insulin-producing beta cells. Melton’s laboratory utilized a virus to perform genetic alterations that are not safe in humans. However, the trials establish the conceptual feasibility of this form of “direct differentiation.” The same method is currently being use for other closely relat cell types, such as liver cells.
Reprogramming
A third strategy is to utilize cells from diabetic patients to generate induce pluripotent stem cells (iPS cells), which are subsequently differentiat into beta cells. The group has already generated several iPS cell lines from diabetes patients with varying genetic origins, but the final process of converting iPS cells into beta cells are not yet suitable for human use.
Self-Regulation
A fourth strategy is not to convert other cells into beta cells, but to stimulate beta cells to multiply. It is now establish, according to studies from the Melton lab, that beta cells in the pancreas do produce more of themselves, although very slowly and at a low rate. With age, this replication becomes slower.
