Liver metabolism in ischemic stroke

Focal brain damage and neurological deficits are the direct consequences of acute ischemic stroke (AIS). In addition, cerebral ischemia causes systemic alterations across peripheral organs. Dysregulation of the autonomic and endocrine systems as well as the release of brain-derived pro-inflammatory mediators trigger a peripheral immune response and systemic inflammation. As a key metabolic organ, the liver contributes not only to post-stroke immunosuppression but also to stress-induced hyperglycemia. At the same time, increased ketogenesis and glutathione production in the liver are likely to combat inflammation and oxidative stress after AIS. The closely linked lipid metabolism could regulate both glucose and glutathione homeostasis. In addition, increased hepatic very low-density lipoprotein (VLDL) secretion may improve the availability of phospholipids, polyunsaturated fatty acids (PUFAs) and glutathione after AIS. This review provides an overview of recent findings concerning ischemic stroke and the liver and discusses the therapeutic potential of targeting the hepatic metabolism to improve patient outcome after stroke.