Brain-derived neurotrophic factor is associated with the
insulin signaling pathway and
glucose tabolism. 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, skeletal 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 (40 ng) 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.