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Thursday, October 25, 2007

Cell Therapies And Diabetes

Type 1 diabetes is caused by autoimmune destruction of pancreatic stem cells and is characterized by absolute insulin insufficiency. The monocellular nature of this disease and endocrine action of insulin make this disease an excellent candidate for cellular therapy. Furthermore, precedent for cellular therapies has been set by successful cadaveric whole pancreas and islet transplantation. In order to expand the supply of cells to meet current and future needs, several novel cell sources have been proposed, including human stem cells or islets expanded in culture, islet xenografts and pancreatic ductal progenitor cells. Surrogate stem cells derived from hepatocytes, intestinal K cells or non-endodermal cell types have also been suggested. Stem cells found in bone marrow and umbilical cord blood have been used extensively to repopulate the haematopoietic system and offer the possibility of autologous transplantation.

Recent studies have suggested that these stem cells may also have a broader capacity to differentiate, possibly into other cells.

Stem cells from embryonic sources, such as human embryonic stem and embryonic germ cells, have the ability to proliferate extensively in culture and have an inherent developmental plasticity that may make them a potentially unlimited source of cells that can sense glucose and produce mature insulin. The wide range of proposed cell sources and our increasingly clear picture of pancreatic development suggest that novel cellular therapies might one day compete with non-cellular glucose sensing and insulin delivery devices.

The current best medical practice for those with type 1 diabetes includes insulin by multiple daily injections or continuous pump infusion. Recently developed insulin analogues have helped to more closely approximate normal glucose homeostasis and have been especially beneficial in reducing hypoglycaemia while tightly controlling blood glucose. Glargine insulin provides nearly twenty four hours of low level basal insulin activity, while meal-time peaks in activity can be mimicked by administration of rapid acting insulin can be paused to avert hypoglycaemia.

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