Researchers at Mayo Clinic found that placing a red blood cell derivative in mice with diabetes could be a solution to delayed gastric emptying. The abnormally high blood glucose levels of gastroparesis cause chemical changes in nerves and in pacemaker cells, which regulate digestive processes in the gut. It also damages blood vessels that carry oxygen and nutrients to cells.
Previous studies in animals and humans showed that gastroparesis exhibits a loss of Kit and a loss of expression of neuronal nitric oxide synthase (nNOS). Kit is a marker for interstitial cells of Cajal (ICC), which 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, a problem common in diabetes that also can lead to heart and kidney damage.
Therefore the team decided to test heme oxygenase-1 (HO1), a molecule known to protect cells against oxidative injury. Investigators induced HO1 production in mice by introducing hemin, which in turn restored the amount of Kit, a marker for ICC, and nNOS. With the changes in expression restored, gastric emptying returned to normal, despite the diabetes.
The findings appear in the online issue of the Gastroenterology.