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Biotech Science

NIH Confirms Protocol To Reverse Type 1 Diabetes 116

FiReaNGeL writes "In 2001, researchers at Massachusetts General Hospital demonstrated the efficacy of a protocol to reverse type 1 diabetes in diabetic mice. New data from a study performed at the National Institutes of Health provides additional confirmation of the ability to reverse type 1 diabetes and on the role of spleen cells in islet regeneration. Spleen cells appear to contribute to islet recovery more in mice who are older and with more advanced diabetes compared with younger mice with less advanced diabetes, in which regeneration of remaining islets may be the dominant mechanism."
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NIH Confirms Protocol To Reverse Type 1 Diabetes

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  • Hype or not? (Score:1, Interesting)

    by El Lobo ( 994537 ) on Saturday November 25, 2006 @09:59AM (#16983742)
    Current investigation, however (both embryonic and adult stem cells), is still in the preliminary stage and several more years remain before they can potentially be used in the clinical setting. Procedures that reduce in vitro manipulation of cells and allow stem cells to develop into islets in vivo are crucial. Furthermore, the regeneration of existing islets is a distinct possibility. Simplistically, it might be hypothesized that down-regulation of autoimmunity may give the pancreas the breathing space to regenerate islets.
  • by retrosteve ( 77918 ) on Saturday November 25, 2006 @12:49PM (#16984630) Homepage Journal
    Ah, but there's another consideration --

    Type 2 diabetes deteriorates if not kept well-controlled. In advanced stages, the hyperglycemia oxidizes proteins and kills off pancreatic islets, until the pancreas is unable to produce insulin, just as in Type 1.

    So if an advanced type-2 diabetic fixed up their insulin resistance, they might still be unable to produce insulin. And the therapy in the article might then be helpful to them too!
  • by Boghog ( 910236 ) on Saturday November 25, 2006 @02:36PM (#16985328)
    the hyperglycemia oxidizes proteins and kills off pancreatic islets, until the pancreas is unable to produce insulin, just as in Type 1.

    You are right on the result (pancreas no longer able to produce insulin), but your mechanism (oxidative stress) is at best only part of the picture. If oxidized proteins induced by hyperglycemia were cytotoxic, a lot more cell types in addition to pancreatic islets would be killed off.

    The exact mechanism of beta cell burn out in advanced type II diabetes is unclear
    http://diabetes.diabetesjournals.org/cgi/content/f ull/54/suppl_2/S108/ [diabetesjournals.org]
    however it certainly related to a prolonged an inappropriately high production of insulin (hyperinsulinemia) in response to high levels blood glucose.

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