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Protein
May Link Obesity To Diabetes
(HealthScoutNews)
-- An overproduction of a protein used by pancreatic cells to
measure blood sugar may explain why those who are overweight are
at risk for type II diabetes, a study in mice suggests.
Should the
same mechanism be at work in humans, the protein -- called uncoupling
protein-2 (UCP2) -- could be a target for new diabetes drugs,
the research suggests.
"Type II diabetes
is caused by two different abnormalities," says Dr. Brad Lowell,
an associate professor at Beth Israel Deaconess Medical Center
in Boston. "One is insulin resistance and the other is pancreatic
beta cell dysfunction. We began to wonder about how beta cells
become dysfunctional, and since type II diabetes is always associated
with obesity, we looked at a mouse model of obesity-induced diabetes."
Type II diabetes
is caused by either a lack of insulin or the inability of cells
to use insulin. When you eat, insulin signals muscle cells to
take up blood sugar and turns off sugar production by the liver.
Type II diabetics have trouble responding to insulin, which causes
the pancreas to manufacture more of the hormone. Eventually the
balance shifts, and the extra insulin can't overcome the insulin
resistance.
The result
is too much sugar in the blood, leading to diabetes and all its
attendant complications -- blindness, heart attack, atherosclerosis,
stroke, kidney failure and nerve damage. An estimated 16 million
Americans have diabetes, and 90 percent of them have type II,
according to the American Diabetes Association. About 80 percent
of type II diabetics are overweight.
Dysfunctional
pancreatic beta cells seem to be at the center of insulin resistance,
Lowell says. Previous research had shown that mice with obesity-induced
diabetes had high levels of the protein in their pancreatic cells,
leading to the suspicion that obesity was linked to the overproduction.
To test the
hypothesis, Lowell and his colleagues created obese mice and removed
a gene preventing the animals from producing UCP2. "When we did
that, we saw that their beta cell function was dramatically improved,
and so was their diabetes," he says. "Potentially decreasing UCP2
by some kind of method could hypothetically prevent type II diabetes,"
he adds.
If UCP2 works
the same way in humans, it could be a breakthrough, Lowell suggests.
"But a lot more work needs to be done to find out if this beta
cell dysfunction operates the same way in other rodent models,
and ultimately humans. It's possible that it may not work the
same way, but that's the next step in research."
The findings
were published in the June 15 issue of Cell.
Lowell's findings
are part of a recent explosion in understanding insulin resistance,
says Dr. Christopher Saudek, president-elect of the American Diabetes
Association and a professor of medicine at Johns Hopkins University.
"There's a huge black box that has just begun to be opened describing
the steps that go on with insulin at the cell surface as well
as the opening of the cell to glucose. These findings are just
one piece of the puzzle, though a potentially very interesting
piece."
Whether this
process works the same way in people is anything but sure, Saudek
says. "It's a big leap to tell whether this is relevant to humans.
The researchers have used a model in which they have done particular
manipulations."
"It's the
next step in research to see if these mechanisms are just as important
in humans," he adds.
What To
Do
For more on
insulin resistance, visit
Diabetes Central. To learn more about the disease, visit the
National Institute of Diabetes and Digestive and Kidney Disorders.
Reference
Source 101
For more information on how to prevent other diseases, use
PreventDisease.com's "Quick
Prevention Resources".
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