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[IP] Research

August 16, 2002

The Juvenile Diabetes Research Foundationbs Research E-Newsletter provides 
all those interested with the latest information about research on type 1 
diabetes and its complications.  Please forward this report to others who may 
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    1. Researchers Identify Key Genetic Switch in Insulin Production
    2. Natural Hormone Can Spur Stem Cell Differentiation
    3. Powerful Tool Developed for Genetics Research
    4. Inhibiting Inflammation May Boost Transplanted Islet Performance

1. Researchers Identify Key Genetic Switch in Insulin Production
Researchers at the Joslin Diabetes Center in Boston have identified a genetic 
switching mechanism needed for the production of insulin in the body. As the 
Boston Globe reported on August 6, the finding could someday lead to a method 
for making insulin-producing cells or even repairing damaged cells inside 
patients. Scientists had known that the gene responsible for making insulin 
was switched on by three proteins, but they did not know exactly how the 
switches were flipped. Two of the chemical switching mechanisms were 
identified in the mid-1990s, but the third had proved elusive. Its discovery 
will provide a boost to researchers investigating ways to convert 
undifferentiated stem cells into insulin producing islet cells. The research, 
reported in the Proceedings of the National Academy of Scientists, was partly 
funded by JDRF.

To read the Boston Globe article about this research, click below:

To read an abstract of this research, click below: 

2. Natural Hormone Can Spur Stem Cell Differentiation
Scientists at Massachusetts General Hospital have found that a naturally 
occurring hormone can prompt adult stem cells in the pancreas to mature into 
insulin-secreting beta cells. The finding, which was made in small animal 
models, could eventually lead to a new strategy for reversing type 1 diabetes 
by creating new insulin-secreting beta cells to replace beta cells destroyed 
by the disease. The research on the hormone is still in early stages, 

The hormone, called glucagon-like peptideb1 (GLPb1), is secreted by the 
lining of the intestine. It was already known that GLPb1 can provoke beta 
cells to proliferate and secrete insulin. Now Joel Habener, M.D., and 
colleagues provide evidence that the hormone also can cause stem cells in the 
pancreas to differentiate into beta cells. This discovery is reported in the 
August issue of the journal Endocrinology. 

To read a press release about this research, click below:
To read an abstract of this research, click below:

3. Powerful Tool Developed for Diabetes-Related Genetics Research
What makes one cell in the body different from another is not the genes it 
contains but which of its genes are turned on, or bexpressed.b The cellbs 
function and fate also are affected by when (and to what degree) this genetic 
expression occurs. Until recently, it was very hard to study genetic 
expression in more than a few genes at once. But scientists have developed a 
powerful tool, called microarray technology, that allows them to determine 
the expression levels of hundreds or thousands of genes in a single 

Now a consortium of researchers at the University of Pennsylvania, Washington 
University, and Harvard University, have developed a microarray specifically 
tailored to type 1 diabetes. This tool, which they call the bPancChip,b 
monitors the expression of genes most relevant to the disease. Researchers 
studying type 1 diabetes will benefit greatly by seeing which genes turn on 
and off in the pancreatic cells as the organ takes shape early in life. At 
precise moments during development, undifferentiated stem cellsbbiological 
blank slatesbare somehow transformed into specialized pancreatic beta cells 
that secrete insulin. 

"The pancreatic chip speeds the discovery of genes involved in getting stem 
cells to differentiate into beta cells,b says Douglas Melton, M.D., a 
JDRF-funded researcher and one of the studybs co-authors.  bInstead of 
testing or looking for genes one at a time, this method allows researchers to 
interrogate thousands of genes at once.b 

The PancChip will be made freely available to members of the research 
community. This tool will help Dr. Melton and other diabetes researchers 
determine which genes control differentiation, when they come into play, and 
how strongly they are expressed. Once they have a comprehensive picture of 
this complex process, scientists can try to mimic the genetic signals in the 
laboratory to artificially coax undifferentiated stem cells to become 
insulin-secreting beta cells. The research was reported in the July issue of 
the journal Diabetes.

To read an abstract of the article, click below

To learn about how microarrays work, click here:

4. Inhibiting Inflammation May Boost Transplanted Islet Performance
A major hurdle in the widespread use of islet transplantation to restore 
blood glucose control is the need for an unexpectedly high number of islets, 
from two or more donors, to produce adequate regulation. Previous research 
has shown that when isolated islets come in direct contact with blood, there 
is a reaction involving inflammation and thrombosis (blood clots). Scientists 
have concluded that this bblood-mediated inflammatory reactionb (IBMIR) 
could be the cause of islet underperformance after transplantation. Now 
researchers in Sweden have set out to see if the reaction could be inhibited. 
They administered an anti-clotting drug, Melagatran, which blocks an enzyme 
called thrombin, which plays a key role in the clotting reaction. They found 
that Melagatran did not affect islet function but did inhibit the 
inflammatory reaction. They suggest that giving the drug during 
transplantation might protect the islets, and that upcoming animal studies 
should indicate whether Melagatran alone is able to control IBMIR or whether 
it should be combined with another drug. The research, reported in the June 
issue of the journal Diabetes, was partly funded by JDRF.

To read the abstract for this study, click below:
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