Ischemic stroke and glucose intolerance: a review of the evidence and exploration of novel therapeutic targets

J Pharmacol Sci. 2012;118(1):1-13. doi: 10.1254/jphs.11r04cr. Epub 2011 Dec 22.


Stroke is one of the leading causes of death and disability worldwide. It is well known that hyperglycemia and/or diabetes potentially exacerbate the neuronal damage observed following ischemic stroke. Recent reports have shown that hyperglycemia/glucose intolerance may be induced by cerebral ischemic stress, and that normalization of blood glucose levels during the first 48 h of hospitalization appears to confer greater survival outcomes in stroke patients. However, the mechanisms underlying post-ischemic glucose intolerance remain unclear. Here, we review research to date on the mechanisms through which ischemic neuronal damage develops and on the role of post-ischemic glucose intolerance focusing on insulin and adiponectin signaling and communication between the brain and peripheral tissues. The relationship between ischemic neuronal damage and post-ischemic glucose intolerance is also discussed. With respect to therapeutic options, in addition to traditional post-stroke therapies, we also discuss the effect of anti-diabetic drugs and glucose-sensing neuropeptides on the development of the post-ischemic glucose intolerance and neuronal damage. In conclusion, we support the idea for focusing research on the development of post-ischemic glucose intolerance as a new therapeutic target for the stroke patients.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Brain Ischemia / complications
  • Brain Ischemia / drug therapy*
  • Brain Ischemia / pathology
  • Diabetes Mellitus / drug therapy
  • Glucose Intolerance / drug therapy*
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Neuroprotective Agents / therapeutic use
  • Risk Factors
  • Stroke / complications
  • Stroke / drug therapy*
  • Stroke / pathology


  • Hypoglycemic Agents
  • Neuroprotective Agents