Hyperglycemia in Stroke Impairs Polarization of Monocytes/Macrophages to a Protective Noninflammatory Cell Type.

Although glucose is the main energy substrate of the brain, hyperglycemia aggravates ischemic brain damage in acute stroke. So far, clinical trials have indicated that insulin treatment provides no solution to this common clinical problem. This study shows, in an experimental stroke model, that hyperglycemia interferes with the polarization of monocytes/macrophages to a protective cell type. Key players are α-dicarbonyls and the receptor for advanced glycation end products (AGER). Deletion of AGER normalized monocyte/macrophage polarization and reversed the detrimental effects of hyperglycemia, suggesting new avenues to treat stroke patients.