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[IPu] ADA: 50 Year Type 1 Diabetes Survivors Show Islet Cells (Medpage)



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     ADA: 50-Year Type 1 Diabetes Survivors Show Islet Cells

        By Neil Osterweil, Senior Associate Editor, MedPage Today
            Reviewed by Zalman S. Agus, MD; Emeritus Professor at the
University of Pennsylvania School of Medicine.
            June 12, 2006


                  MedPage Today Action Points


                    a.. Explain to interested patients that this study raises
the possibility that in some patients with type 1 diabetes, in which
antibodies presumably destroy all of the body's insulin-secreting beta islet
cells, there may be reservoirs of beta cells that could one day be coaxed into
repopulating the pancreas.


                    b.. This study was published as an abstract and presented
orally at a conference. These data and conclusions should be considered to be
preliminary as they have not yet been reviewed and published in a
peer-reviewed publication.


            Review


                  George L. King. M.D.
                  Joslin Diabetes Center
            WASHINGTON, June 12 - After more than half a century of living
with type 1 diabetes, a significant number of patients appear to have residual
beta-islet cell function, according to research presented here.


            In a study of these relatively long-lived type 1 patients about
13% had evidence of C-peptide secretion, indicating that they were still
producing insulin, reported Hillary Keenan, Ph.D., of the Joslin Diabetes
Center in Boston at the American Diabetes Association meeting.


            "It is surprising that some medalists [50-year survivors] still
have C-peptide secretion, a sign of insulin production, and some are positive
for antibodies to the islets, another sign that some islet function of mass
still is present," said George L. King, M.D., the study's lead author.


            The findings suggested that instead of islet cell or pancreas
transplants in people with type 1 diabetes, it might be possible in the future
to stimulate the growth of native, residual islet cells to restore insulin
secretion and glucose regulatory functions to normal levels, Dr. King said.


            In the study, about half the patients had little or no
microvascular complications present, suggesting that diabetes duration does
not always equate to complications.


            The 50-year Medalist Study followed the clinical, physiological,
and genetic characteristics of 326 patients. "The findings are phenomenal,"
Dr. Keenan said. "This is the first study to look at the specific biomarkers
of islet cell presence in people with a 50-year duration of insulin-dependent
diabetes."


            In a subset of 125 of these patients, the investigators found that
12.7% of the patients had a C-peptide level above 0.3 ng/mL, indicating that
they still had a population of active islet cells and some degree of residual
insulin production, despite being dependent on exogenous insulin for most of a
lifetime.


            Still, most of the 50-year survivors had clinical characteristics
typical of type 1 diabetics, regardless of the presence or absence of the
C-peptide.


            Among those patients who were positive for C-peptide, 23.2%
produced either of two common anti-islet antibodies: GADA (glutamic acid
decarboxylase) or IA2 (a tyrosine phosphatase-like protein). The presence of
these antibodies is another indicator that a small pool of islet cells may
still be present and possibly functioning. Otherwise, the antibodies would
presumably have vanished when their target cells died off.


            In addition to looking at C-peptide, the investigators examined
cholesterol and triglycerides levels, body mass index, and daily insulin
requirements, and found that there were no significant differences in these
clinical parameters when controlling for C-peptide presence.


            The lack of microvascular complications in about half of the
patients is particularly intriguing, Dr. King said.


            "If we could find out the reason for their lack of complications,
we could perhaps prevent kidney or eye disease," he commented. "If a way can
be found to stimulate islet growth, we could improve their diabetes and reduce
insulin usage or better control blood glucose levels. If islets were returned
to normal levels, they wouldn't need to take insulin," he said.


            The study was funded by the Joslin Diabetes Research Foundation.

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