title: Pancreatic Changes in Nerve Growth Factor/TrkA Associated with Insulin Secretion in Cerebral Ischemia.
abstract: Regulation of blood glucose levels as a therapeutic strategy for cerebral ischemia plays an important role in suppressing neuronal damage. In particular, suppression of post-ischemic glucose intolerance improves cerebral ischemia. We have reported that cerebral ischemia induces glucose intolerance and an increase in plasma insulin levels. However, the mechanism of insulin secretion after cerebral ischemia is unclear. Nerve growth factor (NGF), a member of the neurotrophin family, has high affinity for tropomyosin-related kinase A (TrkA). NGF/TrkA signaling is associated with neuronal survival, differentiation, and function. Recently, NGF/TrkA signaling has been reported to be associated with insulin synthesis and secretion. In the present study, we evaluated the insulin content and expression of NGF/TrkA by immunofluorescence and Western blotting after middle cerebral artery occlusion (MCAO) as a cerebral ischemia model. At 6, 12, and 24 h after MCAO, insulin contents were increased in MCAO mice. The expression of NGF was increased at 6, 12, and 24 h, whereas the expression of TrkA tended to decrease in pancreas after MCAO. These results suggest that NGF/TrkA signaling is an important factor in cerebral ischemia-induced insulin synthesis and secretion in the pancreas.
authors.affiliation: Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University.
authors.forename: Kei
authors.initials: K
authors.lastname: Miyagi
authors.forename: Shinichi
authors.initials: S
authors.lastname: Harada
authors.forename: Shogo
authors.initials: S
authors.lastname: Tokuyama
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D002470:Cell Survival; D002544:Cerebral Infarction / Q000378:metabolism; D002561:Cerebrovascular Disorders; D004195:Disease Models, Animal; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D008815:Mice, Inbred Strains; D020932:Nerve Growth Factor / Q000378:metabolism*; D009474:Neurons / Q000473:pathology; D010179:Pancreas / Q000378:metabolism*; D020917:Receptor, trkA / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020932:Nerve Growth Factor; D020917:Receptor, trkA