Guest guest Posted March 12, 2012 Report Share Posted March 12, 2012 Interesting article, but I still wonder if the immune system would eventually attack those cells too. _____ From: blind-diabetics [mailto:blind-diabetics ] On Behalf Of armando del gobbo Sent: Monday, March 12, 2012 11:35 AM To: blind-diabetics Subject: Maybe something new? > New Approach to Treating Type 1 Diabetes? Transforming Gut Cells Into > Insulin Factories > ScienceDaily (Mar. 11, 2012) ? A study by Columbia researchers suggests > that cells in the patient's intestine could be coaxed into making insulin, > circumventing the need for a stem cell transplant. Until now, stem cell > transplants have been seen by many researchers as the ideal way to replace > cells lost in type I diabetes and to free patients from insulin > injections. > See Also: > The research -- conducted in mice -- was published 11 March 2012 in the > journal Nature Genetics. > Type I diabetes is an autoimmune disease that destroys insulin-producing > cells in the pancreas. The pancreas cannot replace these cells, so once > they are lost, people with type I diabetes must inject themselves with > insulin to control their blood glucose. Blood glucose that is too high or > too low can be life threatening, and patients must monitor their glucose > several times a day. > A longstanding goal of type I diabetes research is to replace lost cells > with new cells that release insulin into the bloodstream as needed. Though > researchers can make insulin-producing cells in the laboratory from > embryonic stem cells, such cells are not yet appropriate for transplant > because they do not release insulin appropriately in response to glucose > levels. If these cells were introduced into a patient, insulin would be > secreted when not needed, potentially causing fatal hypoglycemia. > The study, conducted by Chutima Talchai, PhD, and Domenico Accili, MD, > professor of medicine at Columbia University Medical Center, shows that > certain progenitor cells in the intestine of mice have the surprising > ability to make insulin-producing cells. Dr. Talchai is a postdoctoral > fellow in Dr. Accili's lab. > The gastrointestinal progenitor cells are normally responsible for > producing a wide range of cells, including cells that produce serotonin, > gastric inhibitory peptide, and other hormones secreted into the GI tract > and bloodstream. > Drs. Talchai and Accili found that when they turned off a gene known to > play a role in cell fate decisions -- Foxo1 -- the progenitor cells also > generated insulin-producing cells. More cells were generated when Foxo1 > was turned off early in development, but insulin-producing cells were also > generated when the gene was turned off after the mice had reached > adulthood. " Our results show that it could be possible to regrow > insulin-producing cells in the GI tracts of our pediatric and adult > patients, " Dr. Accili says. > " Nobody would have predicted this result, " Dr. Accili adds. " Many things > could have happened after we knocked out Foxo1. In the pancreas, when we > knock out Foxo1, nothing happens. So why does something happen in the gut? > Why don't we get a cell that produces some other hormone? We don't yet > know. " > Insulin-producing cells in the gut would be hazardous if they did not > release insulin in response to blood glucose levels. But the researchers > say that the new intestinal cells have glucose-sensing receptors and do > exactly that. > The insulin made by the gut cells also was released into the bloodstream, > worked as well as normal insulin, and was made in sufficient quantity to > nearly normalize blood glucose levels in otherwise diabetic mice. > " All these findings make us think that coaxing a patient's gut to make > insulin-producing cells would be a better way to treat diabetes than > therapies based on embryonic or iPS stem cells, " Dr. Accili says. The > location of the cells in the gut may also prevent the diabetes from > destroying the new insulin-producing cells, since the gastrointestinal > tract is partly protected from attack by the immune system. > The key to turning the finding into a viable therapy, Dr. Accili says, > will be to find a drug that has the same effect on the gastrointestinal > progenitor cells in people as knocking out the Foxo1 gene does in mice. > That should be possible, he says, since the researchers found that they > could also create insulin-producing cells from progenitor cells by > inhibiting Foxo1 with a chemical. > " It's important to realize that a new treatment for type I diabetes needs > to be just as safe as, and more effective than, insulin, " Dr. Accili says. > " We can't test treatments that are risky just to remove the burden of > daily injections. Insulin is not simple or perfect, but it works and it is > safe. " > The research was supported by the NIH (DK58282, DK64819, DK63608), the New > York Stem Cell Foundation, and the Berrie Foundation. > > > > ------------------------------------ > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 12, 2012 Report Share Posted March 12, 2012 well, I, as both a kidney and pancreas transplant patient, I have to keep my immune system down and the anti rejections meds I take help do that,thus keeping my transplanted organs " dormant " in order for them to keep functioning. " The LORD is my light and my salvation - so why should I be afraid? The Lord is my fortress, protecting me from danger, so why should I tremble? " ~Psalm 27:1 ~Be Blessed, Sugar Maybe something new? > New Approach to Treating Type 1 Diabetes? Transforming Gut Cells Into > Insulin Factories > ScienceDaily (Mar. 11, 2012) ? A study by Columbia researchers suggests > that cells in the patient's intestine could be coaxed into making insulin, > circumventing the need for a stem cell transplant. Until now, stem cell > transplants have been seen by many researchers as the ideal way to replace > cells lost in type I diabetes and to free patients from insulin > injections. > See Also: > The research -- conducted in mice -- was published 11 March 2012 in the > journal Nature Genetics. > Type I diabetes is an autoimmune disease that destroys insulin-producing > cells in the pancreas. The pancreas cannot replace these cells, so once > they are lost, people with type I diabetes must inject themselves with > insulin to control their blood glucose. Blood glucose that is too high or > too low can be life threatening, and patients must monitor their glucose > several times a day. > A longstanding goal of type I diabetes research is to replace lost cells > with new cells that release insulin into the bloodstream as needed. Though > researchers can make insulin-producing cells in the laboratory from > embryonic stem cells, such cells are not yet appropriate for transplant > because they do not release insulin appropriately in response to glucose > levels. If these cells were introduced into a patient, insulin would be > secreted when not needed, potentially causing fatal hypoglycemia. > The study, conducted by Chutima Talchai, PhD, and Domenico Accili, MD, > professor of medicine at Columbia University Medical Center, shows that > certain progenitor cells in the intestine of mice have the surprising > ability to make insulin-producing cells. Dr. Talchai is a postdoctoral > fellow in Dr. Accili's lab. > The gastrointestinal progenitor cells are normally responsible for > producing a wide range of cells, including cells that produce serotonin, > gastric inhibitory peptide, and other hormones secreted into the GI tract > and bloodstream. > Drs. Talchai and Accili found that when they turned off a gene known to > play a role in cell fate decisions -- Foxo1 -- the progenitor cells also > generated insulin-producing cells. More cells were generated when Foxo1 > was turned off early in development, but insulin-producing cells were also > generated when the gene was turned off after the mice had reached > adulthood. " Our results show that it could be possible to regrow > insulin-producing cells in the GI tracts of our pediatric and adult > patients, " Dr. Accili says. > " Nobody would have predicted this result, " Dr. Accili adds. " Many things > could have happened after we knocked out Foxo1. In the pancreas, when we > knock out Foxo1, nothing happens. So why does something happen in the gut? > Why don't we get a cell that produces some other hormone? We don't yet > know. " > Insulin-producing cells in the gut would be hazardous if they did not > release insulin in response to blood glucose levels. But the researchers > say that the new intestinal cells have glucose-sensing receptors and do > exactly that. > The insulin made by the gut cells also was released into the bloodstream, > worked as well as normal insulin, and was made in sufficient quantity to > nearly normalize blood glucose levels in otherwise diabetic mice. > " All these findings make us think that coaxing a patient's gut to make > insulin-producing cells would be a better way to treat diabetes than > therapies based on embryonic or iPS stem cells, " Dr. Accili says. The > location of the cells in the gut may also prevent the diabetes from > destroying the new insulin-producing cells, since the gastrointestinal > tract is partly protected from attack by the immune system. > The key to turning the finding into a viable therapy, Dr. Accili says, > will be to find a drug that has the same effect on the gastrointestinal > progenitor cells in people as knocking out the Foxo1 gene does in mice. > That should be possible, he says, since the researchers found that they > could also create insulin-producing cells from progenitor cells by > inhibiting Foxo1 with a chemical. > " It's important to realize that a new treatment for type I diabetes needs > to be just as safe as, and more effective than, insulin, " Dr. Accili says. > " We can't test treatments that are risky just to remove the burden of > daily injections. Insulin is not simple or perfect, but it works and it is > safe. " > The research was supported by the NIH (DK58282, DK64819, DK63608), the New > York Stem Cell Foundation, and the Berrie Foundation. > > > > ------------------------------------ > > Quote Link to comment Share on other sites More sharing options...
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