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Discovery
may help Diabetic Gastric Problem
Newswise — Mayo Clinic researchers have
found what may provide a solution to one of
the more troubling complications of diabetes
-- delayed gastric emptying or gastroparesis.
The researchers showed in animal models that
a red blood cell derivative increases
production of a key molecule, normalizing
the digestive process.
he findings appear in the current online
issue of the journal Gastroenterology (http://www.gastrojournal.org/
).
Gastroparesis occurs when the stomach
retains food for longer periods. When that
food eventually passes into the small
intestine, insulin is released.
Because the passage of food out of the
stomach becomes unpredictable, maintaining a
proper blood glucose level -- critical for
controlling diabetes -- also becomes
difficult.
Gastroparesis can cause pain, nausea,
vomiting, stomach spasms and weight loss due
to inadequate absorption of nutrients.
The abnormally high blood glucose levels
cause chemical changes in nerves and in
pacemaker cells which regulate digestive
processes in the gut, and damage blood
vessels that carry oxygen and nutrients to
cells.
“If these data are confirmed in humans, it
may point toward a treatment for this
difficult problem,” says Gianrico Farrugia,
M.D., Mayo Clinic gastroenterologist and
senior author on the study.
“Our
goal is to normalize gastric emptying and
therefore improve a patient’s quality of
life and glucose control.”
Science Behind the Findings
Previous studies in animals and humans
showed that two aspects of gastroparesis
were: 1) loss of Kit, a marker for
interstitial cells of Cajal (ICC), and 2)
loss of expression of neuronal nitric oxide
synthase (nNOS).
ICC cells produce electrical signals that
regulate muscle contraction in the digestive
tract. nNOS generates nitric oxide, which
transmits nerve impulses in the digestive
tract.
Both are important for normal functioning
but can be depleted by oxidative stress (an
imbalance in ionic charges at the molecular
level), a problem common in diabetes that
also can lead to heart and kidney damage.
The research team decided to test a molecule
known to protect cells against oxidative
injury -- heme oxygenase-1 (HO1).
The team measured gastric emptying in a set
of diabetic mice and then looked at
expression of HO1. Results showed that
production of HO1 was lost in all mice with
gastroparesis and nNOS expression was
decreased.
When the team induced HO1 production by
introducing hemin, a red blood derivative,
gastric emptying returned to normal and Kit
and nNOS expression were restored, despite
the diabetes.
The team says that future research should
target the HO1 pathway as a means of
reversing the affects of diabetic
gastroparesis.
Others researchers were Kyoung Moo Choi,
Ph.D.; Simon Gibbons, Ph.D.; Tien Hguyen;
Gary Stoltz; Matthew Lurken; Tamas Ordog,
M.D.; and Joseph Szurszewski, Ph.D., all of
Mayo Clinic. The research was funded by the
National Institutes of Health.
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