Brain-derived neurotrophic factor is associated with the insulin signaling pathway and glucose metabolism.We hypothesized that expression of brain-derived neurotrophic factor and its receptor may be involved in glucose intolerance following ischemic stress.To verify this hypothesis,this study aimed to observe the changes in brain-derived neurotrophic factor and tyrosine kinase B receptor expression in glucose metabolism-associated regions following cerebral ischemic stress in mice.At day 1 after middle cerebral artery occlusion,the expression levels of brain-derived neurotrophic factor were significantly decreased in the ischemic cortex,hypothalamus,liver,skeleta muscle,and pancreas.The expression levels of tyrosine kinase B receptor were decreased in the hypothalamus and liver,and increased in the skeletal muscle and pancreas,but remained unchanged in the cortex.Intrahypothalamic administration of brain-derived neurotrophic factor(40ng)suppressed the decrease in insulin receptor and tyrosine-phosphorylated insulin receptor expression in the liver and skeletal muscle,and inhibited the overexpression of gluconeogenesis-associated phosphoenolpyruvate carboxykinase and glucose-6-phosphatase in the liver of cerebral ischemic mice.However,serum insulin levels remained unchanged.Our experimental findings indicate that brain-derived neurotrophic factor can promote glucose metabolism,reduce gluconeogenesis,and decrease blood glucose levels after cerebral ischemic stress.The low expression of brain-derived neurotrophic factor following cerebral ischemia may be involved in the development of glucose intolerance. Brain-derived neurotrophic factor is associated with the insulin signaling pathway and glucose metabolism. We hypothesized that expression of brain-derived neurotrophic factor and its receptor may be involved in glucose intolerance following ischemic stress. To verify this hypothesis, this study aimed to observe the changes in brain-derived neurotrophic factor and tyrosine kinase B receptor expression in glucose metabolism-associated regions following cerebral ischemic stress in mice. At day 1 after middle cerebral artery occlusion, the expression levels of brain-derived neurotrophic factor were significantly decreased in the ischemic cortex, hypothalamus, liver, skeleta muscle, and pancreas. The expression levels of tyrosine kinase B receptor were decreased in the hypothalamus and liver, and increased in the skeletal muscle and pancreas, but remained unchanged in the cortex. Intranypothalamic administration of brain-derived The neurotrophic factor (40ng) suppressed the decrease in insulin receptor and t yrosine-phosphorylated insulin receptor expression in the liver and skeletal muscle, and inhibited the overexpression of gluconeogenesis-associated phosphoenolpyruvate carboxykinase and glucose-6-phosphatase in the liver of cerebral ischemic mice. However, serum insulin levels were unchanged unchanged. Our experimental findings indicate that that brain-derived neurotrophic factor can promote glucose metabolism, reduce gluconeogenesis, and decrease blood glucose levels following cerebral ischemic stress. The low expression of brain-derived neurotrophic factor following cerebral ischemia may be involved in the development of glucose intolerance.