Hyperglycemia results from impaired insulin activity and is a hallmark of diabetes.
Researchers led by Chih-Hao Li at Harvard University identified IL-13, a protein more commonly associated with the immune system, as a regulator of blood glucose levels. Mice lacking IL-13 had higher blood sugar and lipid levels compared with normal mice, and exhibited glucose intolerance and insulin resistance.
Treatment with recombinant IL-13 reversed these effects. Li and colleagues found that IL-13 repressed glucose production in the liver, contributing to lower blood sugar levels.