Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/94827
DC FieldValueLanguage
dc.contributor.authorChen, Wen-Yingzh_TW
dc.contributor.authorMao, Frank Chiahungzh_TW
dc.contributor.authorLiu, Chia-Hsinzh_TW
dc.contributor.authorKuan, Yu-Hsiangzh_TW
dc.contributor.authorLai, Nai-Weizh_TW
dc.contributor.authorWu, Chih-Chengzh_TW
dc.contributor.authorChen, Chun-Jungzh_TW
dc.date2016-04-
dc.date.accessioned2018-04-30T07:48:13Z-
dc.date.available2018-04-30T07:48:13Z-
dc.identifier.urihttp://hdl.handle.net/11455/94827-
dc.description.abstractHyperglycemia is common after acute stroke and is associated with a worse outcome of stroke. Thus, a better understanding of stress hyperglycemia is helpful to the prevention and therapeutic treatment of stroke. Chromium is an essential nutrient required for optimal insulin activity and normal carbohydrate and lipid metabolism. Beyond its nutritional effects, dietary supplement of chromium causes beneficial outcomes against several diseases, in particular diabetes-associated complications. In this study, we investigated whether post-stroke hyperglycemia involved chromium dynamic mobilization in a rat model of permanent focal cerebral ischemia and whether dietary supplement of chromium improved post-stroke injury and alterations. Stroke rats developed brain infarction, hyperglycemia, hyperinsulinemia, glucose intolerance, and insulin resistance. Post-stroke hyperglycemia was accompanied by elevated secretion of counter-regulatory hormones including glucagon, corticosterone, and norepinephrine, decreased insulin signaling in skeletal muscles, and increased hepatic gluconeogenesis. Correlation studies revealed that counter-regulatory hormone secretion showed a positive correlation with chromium loss and blood glucose increased together with chromium loss. Daily chromium supplementation increased tissue chromium levels, attenuated brain infarction, improved hyperglycemia, and decreased plasma levels of glucagon and corticosterone in stroke rats. Our findings suggest that stroke rats show disturbance of tissue chromium homeostasis with a net loss through urinary excretion and chromium mobilization and loss might be an alternative mechanism responsible for post-stroke hyperglycemia.zh_TW
dc.language.isoenzh_TW
dc.relationMetabolic brain disease, Volume 31, Issue 2, Page(s) 289-97.zh_TW
dc.subjectChromiumzh_TW
dc.subjectCounter-regulatory hormoneszh_TW
dc.subjectHyperglycemiazh_TW
dc.subjectStrokezh_TW
dc.subjectAnimalszh_TW
dc.subjectBlood Glucosezh_TW
dc.subjectBrain Ischemiazh_TW
dc.subjectChromiumzh_TW
dc.subjectDiabetes Mellitus, Experimentalzh_TW
dc.subjectHyperglycemiazh_TW
dc.subjectHypoglycemic Agentszh_TW
dc.subjectInsulin Resistancezh_TW
dc.subjectMalezh_TW
dc.subjectRats, Sprague-Dawleyzh_TW
dc.subjectStrokezh_TW
dc.subjectDietary Supplementszh_TW
dc.titleChromium supplementation improved post-stroke brain infarction and hyperglycemiazh_TW
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1007/s11011-015-9749-yzh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.fulltextno fulltext-
item.cerifentitytypePublications-
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