Insulin-producing beta-cells can proliferate by making more of themselves, research in this week's Nature (VOL. 429 NO. 6987 DATED 6 MAY 2004, pp. 41-46) suggests. The study, which counters the prevailing hypothesis on beta-cell production, may aid the development of new treatments for type I diabetes.
Once we've eaten, we store any excess sugar in order to reserve energy for later. Excess glucose is sensed by beta-cells in the pancreas, which respond by secreting the hormone insulin into the bloodstream. Insulin, in turn, tells various cells in the body to store glucose. In type I diabetes, the immune system destroys beta-cells, resulting in a lifelong dependency on insulin therapy. So researchers have long been searching for a renewable source of transplantable beta-cells.
Douglas A. Melton and colleagues used a genetic approach for marking cells and tracing their fate, to shed light on the origin of beta-cells in adult mice. They find that beta-cells arise mainly from pre-existing beta-cells and not from pancreatic stem cells, as was previously thought.
If human beta-cells replicate like their mouse counterparts, then the discovery may prompt the development of new therapies for type I diabetes, says Ken Zaret in an accompanying News and Views article. "It doesn't exclude the possibility that, in some diseases, adult stem cells might contribute to the beta-cell population. But it does shine light on a resource for insulin-producing cells that has been there all along: the beta-cell itself."
Douglas A. Melton (HHMI, Harvard University, Cambridge, MA, USA)
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Ken Zaret (Fox Chase Cancer Center, Philadelphia, PA, USA)
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(C) Nature press release.
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