Washington, March 20 ANI | 6 months ago

Researchers have found proof that the insulin-secreting beta cells of the pancreas, which are either killed or become dysfunctional in the two main forms of diabetes, have the capacity to regenerate.


Alvin Powers, M.D., the paper's senior author and director of the Vanderbilt Diabetes Center, said that the study "provides clues to how we might learn what signals promote beta-cell regeneration in type 1 and type 2 diabetes."

In the past three months, the Powers group at Vanderbilt, in four separate papers, has reported important findings about the "microenvironment" of the insulin-secreting beta cells and glucagon-secreting alpha cells, which are among four types of cells clustered in "islets" in the pancreas.

In two papers in the journal Diabetes and one each in Development and Cell Metabolism, the researchers described four main findings about islet vascularization and innervation:
First, vascular endothelial growth factor A (VEGF-A) is important for development of the islets' blood supply and for beta-cell proliferation. Blocking the growth factor early in development in a mouse model ultimately reduced beta-cell mass and insulin release and impaired glucose clearance from the bloodstream.

Second, VEGF and other "signals" released by the endothelial cells lining islet blood vessels consequently stimulated growth of islet nerves in mice that connected to the brain.

Third, VEGF-A was not involved when the beta-cell mass increased in an obese mouse model of type 2 diabetes in response to rising glucose levels.

Unlike tumors, which sprout new blood vessels as they grow, the beta-cell tissue increased its blood supply by dilating existing vessels.

Finally, too much VEGF-A can lead to beta cell death. But that sets up a regenerative microenvironment involving an interaction of vascular endothelial cells and macrophages which, in turn, leads to beta cell proliferation both in mice and human islets.

The findings have been published online in the journal Cell Metabolism.

(Posted on 20-03-2014)

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