Résumé
In the original publication, the author name was incorrectly published as "Lifeng Chen".
Résumé
Zinc-α2-glycoprotein (ZAG), encoded by the AZGP1 gene, is a major histocompatibility complex I molecule and a lipid-mobilizing factor. ZAG has been demonstrated to promote lipid metabolism and glucose utilization, and to regulate insulin sensitivity. Apart from adipose tissue, skeletal muscle, liver, and kidney, ZAG also occurs in brain tissue, but its distribution in brain is debatable. Only a few studies have investigated ZAG in the brain. It has been found in the brains of patients with Krabbe disease and epilepsy, and in the cerebrospinal fluid of patients with Alzheimer disease, frontotemporal lobe dementia, and amyotrophic lateral sclerosis. Both ZAG protein and AZGP1 mRNA are decreased in epilepsy patients and animal models, while overexpression of ZAG suppresses seizure and epileptic discharges in animal models of epilepsy, but knowledge of the specific mechanism of ZAG in epilepsy is limited. In this review, we summarize the known roles and molecular mechanisms of ZAG in lipid metabolism and glucose metabolism, and in the regulation of insulin sensitivity, and discuss the possible mechanisms by which it suppresses epilepsy.
Sujets)
Animaux , Humains , Adipocytes , Métabolisme , Encéphale , Métabolisme , Protéines de transport , Métabolisme , Épilepsie , Métabolisme , Glucose , Métabolisme , Glycoprotéines , Métabolisme , Insulinorésistance , Métabolisme lipidique , Neurones , Métabolisme , Transduction du signalRésumé
Hyperglycemia is common in patients with aneurysmal subarachnoid hemorrhage (aSAH),and it has important association with dehyed cerebral ischemia (DCI) and may result in poor prognosis.This article summarizes the mechanism of the elevated blood glucose after aSAH,the reasons of causing DCI,and the corresponding treatment measures.