Wednesday, February 20, 2008

Embryonic Stem Cells and Diabetes

Yesterday I noted an article that helped shed light on the evolutionary history of the development of metabolic disorders. Today we hear the exciting news that researchers at the biotech company Novocell have been able to convert embryonic stem cells into cells that produce insulin for mice. The NY Times has the scoop here, and here is a sample:

Scientists reported on Wednesday that they were able to control diabetes in mice by harnessing human embryonic stem cells. The work raised the prospect that the embryonic cells might one day be used to provide insulin-producing replacement cells to treat the disease in people.

The scientists, at the biotechnology company Novocell, turned the stem cells into cells that produced insulin in the mice. Those cells kept blood sugar in check after the mice’s own insulin-producing cells were destroyed.

“For those who say there is not much evidence that embryonic stem cells can cure diabetes, there you go,” said Dr. Camillo Ricordi, director of the Diabetes Research Institute at the University of Miami, who was not involved in the research.

The study is published on the advanced online publication of Nature Biotechnology. Here is the abstract:

Pancreatic endoderm derived from human embryonic stem cells generates glucose-responsive insulin-secreting cells in vivo

By Evert Kroon, et. al.

Development of a cell therapy for diabetes would be greatly aided by a renewable supply of human -cells. Here we show that pancreatic endoderm derived from human embryonic stem (hES) cells efficiently generates glucose-responsive endocrine cells after implantation into mice. Upon glucose stimulation of the implanted mice, human insulin and C-peptide are detected in sera at levels similar to those of mice transplanted with 3,000 human islets. Moreover, the insulin-expressing cells generated after engraftment exhibit many properties of functional -cells, including expression of critical -cell transcription factors, appropriate processing of proinsulin and the presence of mature endocrine secretory granules. Finally, in a test of therapeutic potential, we demonstrate that implantation of hES cell–derived pancreatic endoderm protects against streptozotocin-induced hyperglycemia. Together, these data provide definitive evidence that hES cells are competent to generate glucose-responsive, insulin-secreting cells.

Lets hope a story like this can revive our optimism for scientific research and help topple the dogma and arrogance that has restrained stem cell research.