NEW YORK (Reuters Health) - Mice lacking the gene for macrophage migration inhibitory factor (MIF) are resistant to an experimental form of type 1 diabetes, according to study findings presented Thursday at the 229th national meeting of the American Chemical Society (ACS) in San Diego.
Despite its name, MIF has several pro-inflammatory properties. As such, the protein may recruit immune cells to the pancreas and induce chemical changes that damage the islet cells and their ability to produce insulin.
In a previous study, Dr. Yousef Al-Abed, from North Shore-Long Island Jewish Health System in Manhasset, New York, and colleagues showed that MIF levels are elevated in diabetic animals, and last year at the ACS meeting, they described how blocking MIF with a chemical called ISO-1 prevented diabetes in mice.
This latter finding led the researchers to examine the effects of deleting the MIF gene in mice exposed to multiple low doses of streptozotocin, a model for type 1 diabetes. They found that wild-type mice developed diabetes as expected, whereas MIF-null mice were protected from the endocrine disease.
MIF could represent a viable target for therapeutic interventions, Dr. Al-Abed told Reuters Health. “We’ve already developed a number of compounds that are more effective than ISO-1 in blocking MIF,” he added.
“However, before beginning clinical trials of these compounds, we have to confirm that MIF levels are actually elevated in humans with type 1 diabetes,” Dr. Al-Abed noted. In addition, further animal studies are needed to determine if these compounds are useful for treating as well as preventing type 1 diabetes and whether they have any activity against type 2 diabetes, he added.
MeSH Headings:Animal Diseases: Biological Therapy: Diabetes Mellitus, Experimental: Disease Models, Animal: Genetic Engineering: Genetic Techniques: Investigative Techniques: Therapeutics: Gene Therapy: Analytical, Diagnostic and Therapeutic Techniques and Equipment: DiseasesCopyright © 2002 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.
