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|標題:||Chromium supplementation improved post-stroke brain infarction and hyperglycemia||作者:||Chen, Wen-Ying
Mao, Frank Chiahung
|關鍵字:||Chromium;Counter-regulatory hormones;Hyperglycemia;Stroke;Animals;Blood Glucose;Brain Ischemia;Chromium;Diabetes Mellitus, Experimental;Hyperglycemia;Hypoglycemic Agents;Insulin Resistance;Male;Rats, Sprague-Dawley;Stroke;Dietary Supplements||Project:||Metabolic brain disease, Volume 31, Issue 2, Page(s) 289-97.||摘要:||
Hyperglycemia 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.
|Appears in Collections:||獸醫學系所|
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