Researchers from Washington University School of Medicine in St. Louis have isolated a potential trigger of chronic inflammation that may underlie the various complications associated with diabetes. The discovery in mouse models was that by blocking the production of fat in specific immune cells, the mice did not develop insulin resistance, diabetes, and chronic inflammation, even in the presence of a high-fat diet. Senior investigator Clay F. Semenkovich, MD, the Irene E. and Michael M. Karl Professor and director of the Division of Endocrinology, Metabolism & Lipid Research at the School of Medicine, observed, “We have made modest progress in making it less likely for some people with diabetes to have heart attacks and strokes. However, those receiving optimal therapy are still much more likely to die from complications driven by chronic inflammation that is, at least in part, generated by these immune cells.” The findings were reported online last week in the journal Nature.
In the study, mice were genetically engineered to be unable to produce the enzyme for fatty acid synthase (FAS) in macrophages. It was found that if these immune cells could not synthesize fat from within, their external membranes did not respond to fat from outside, thereby preventing them from contributing to inflammation. In translating the work to clinically relevant treatments the authors say that it will be necessary to develop a means to inhibit fatty acid synthase in the macrophages without eliminating their ability to fight infections.
Read a news story about the discovery, with a link to the journal article, here.
Posted on November 6, 2016