title: Ischemia-induced hyperglycemia: consequences, neuroendocrine regulation, and a role for RAGE.
abstract: Many patients that present with cerebral ischemia exhibit moderate to severe hyperglycemia. Although many hyperglycemic patients suffer from diagnosed or previously undiagnosed diabetes a further subset of individuals is hyperglycemic without diabetes. Hyperglycemia during cerebral ischemia is associated with high levels of mortality and morbidity and limits the effective treatment interventions available. Controlling hyperglycemia with insulin treatment in critical care situations improves overall outcomes, although it is not without risk. Therefore it is critically important to understand the basic mechanisms that underlie both the induction of hyperglycemia and the consequences of it for ischemic outcomes. In this manuscript, the neuroendocrine mediators, and mechanisms of hyperglycemia exacerbated inflammation, glucose dysregulation and ischemic outcomes are discussed. The possibility that the advanced glycation end product (AGE) and receptor for AGE (RAGE) axis mediates the deleterious effects of hyperglycemia on inflammation and neuronal damage is discussed.
authors.affiliation: Department of Neuroscience, Ohio State University Medical Center, Columbus, OH 43210, USA. Zachary.weil@osumc.edu
authors.forename: Zachary M
authors.initials: ZM
authors.lastname: Weil
mesh_terms: D000818:Animals; D001786:Blood Glucose; D002545:Brain Ischemia / Q000150:complications* / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology* / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism*; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic