Diabetes, a disease with 346 million sufferers worldwide, is a significant health and welfare problem that the modern society faces. The pancreas is made from two distinct components: the exocrine pancreas, a reservoir of digestive enzymes, and the endocrine islets the source of the vital metabolic hormone insulin. Human islets possess limited regenerative ability; loss of islet ß-cells in diseases such as type 1 diabetes requires therapeutic intervention.the leading strategy for restoration of ß-cell mass is through the generation and transplantation of new ß-cells derived from human pluripotent stem cells. Other approaches include stimulating endogenous ß-cell proliferation, reprogramming non ß-cells to ß like cells, and harvesting islets from genetically engineered animals. Together these approaches form genetically engineered animals. Together these approaches form a rich pipeline of therapeutic development for pancreatic regeneration.
At present, however, transplantation therapy has the problem of an acute shortage of donor organs or tissues. An innovative study has recently been conducted showing that it may be possible to induce pancreatic regeneration. There is a long history of investigations into pancreatic regeneration, going back nearly a century. The epidemic of diabetes in recent decades has spurred numerous studies on pancreas development, homeostasis, and regeneration. Animal studies have suggested that the exocrine pancreas possesses an intrinsic capacity for regeneration and thus can make a rapid and full recovery from exocrine diseases such as acute pancreatitis. By contrast, the endocrine islets have limited regenerative capacity in adults. Indeed, it remains unclear whether the adult human pancreas can spontaneously regenerate ß-cells in any physiologically meaningful way. Substantial ß-cell loss therefore results in permanent endocrine deficiency and irreversible diabetes. There is an increasing consensus that a regenerative medicine approach will be helpful, even essential, in treating certain forms of diabetes including T1D and possibly the subset of T2D in which there is substantial ß-cell loss.