Hunger Hormone Key to Treating Reperfusion Injury
Scientists at The Feinstein Institute for Medical Research have used the hunger hormone Ghrelin to block organ injury after intestinal ischemia-reperfusion, a common surgical problem with a high risk of death.
Manhasset, NY (Vocus/PRWEB ) May 7, 2008 -- Scientists at The Feinstein Institute for Medical Research have used the hunger hormone Ghrelin to block organ injury after intestinal ischemia-reperfusion, a common surgical problem with a high risk of death.
Ping Wang, MD, and his colleagues used Ghrelin, which has potent anti-inflammatory properties, in laboratory models to test its effects on the events that take place on the heels of oxygen deprivation in the gut. They found that it worked to dramatically protect against the abnormal inflammatory cascade that occurs when oxygen is restored to the tissue. The study was published in PLoS One.
Ghrelin was discovered in 1999 by Kenji Kangawa, MD, and his colleagues at the Miyazaki Department of Biochemistry and the National Cardiovascular Center Research Institute in Japan; it was initially linked to satiety and the regulation of energy balance. Since then, scientists have discovered that the hormone wears many hats in biology, including one that involves inflammation. Ghrelin is found primarily in the gastrointestinal tract.
During abdominal emergency surgery, there is a risk that the blood supply feeding the intestine can be temporarily blocked, setting in motion a potentially life-threatening problem. Once blood flow is restored, the reperfusion of oxygen triggers white blood cells to move into the area and release molecules that can damage local tissue. Dr. Wang and his colleagues found previously that Ghrelin levels in the circulation decrease dramatically during ischemia-reperfusion, so he decided to inject it into laboratory models to document what happens. They found that it decreased the abnormal inflammatory response –- the surge of cytokines and neutrophils -- by more than 50 percent, improved the function of the gut and reduced the bacterial count in the intestine. Lung injury, another problem triggered by reperfusion, was also significantly reduced.
“Intestinal ischemia-reperfusion is a very critical condition, and there are no treatments,” said Dr. Wang. “Hopefully, we can work towards developing this into an effective treatment for patients.” More laboratory work is required before scientists move into clinical trials.
Contact:
Jamie Talan
science writer-in-residence
516-562-1232 (p)
631-682-8781 (c)
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