Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/67865
標題: Adipose proinflammatory cytokine expression through sympathetic system is associated with hyperglycemia and insulin resistance in a rat ischemic stroke model
作者: Wang, Y.Y.
Lin, S.Y.
Chuang, Y.H.
Chen, C.J.
Tung, K.C.
Sheu, W.H.H.
關鍵字: monocyte chemoattractant protein-1
sympathetic nervous system
tumor
necrosis factor-alpha
tumor-necrosis-factor
monocyte chemoattractant protein-1
induced
inflammation
glucose-metabolism
3t3-l1 adipocytes
factor-alpha
tissue
obesity
stress
brain
期刊/報告no:: American Journal of Physiology-Endocrinology and Metabolism, Volume 300, Issue 1, Page(s) E155-E163.
摘要: Wang YY, Lin SY, Chuang YH, Chen CJ, Tung KC, Sheu WH. Adipose proinflammatory cytokine expression through sympathetic system is associated with hyperglycemia and insulin resistance in a rat ischemic stroke model. Am J Physiol Endocrinol Metab 300: E155-E163, 2011. First published October 26, 2010; doi:10.1152/ajpendo.00301.2010.Patients who experience acute ischemic stroke may develop hyperglycemia, even in the absence of diabetes, but the exact mechanisms are still unclear. Adipose tissue secretes numerous proinflammatory cytokines and is involved in the regulation of glucose metabolism. This study aimed to determine the effects of acute stroke on adipose inflammatory cytokine expression. In addition, because sympathetic activity is activated after acute stroke and catecholamines can regulate the expression of several adipocytokines, this study also evaluated whether alterations in adipose proinflammatory cytokines following acute stroke, if any, were medicated by sympathetic system. Acute ischemic brain injury was induced by ligating the right middle cerebral artery and bilateral common carotid arteries in male adult Sprague-Dawley rats. Adipose tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) mRNA and protein levels were determined by RT-PCR and enzyme-linked immunoassay, respectively. The stroke rats developed glucose intolerance on days 1 and 2 after cerebral ischemic injury. The fasting blood insulin levels and insulin resistance index measured by homeostasis model assessment were higher in the stroke rats compared with the sham group. Epididymal adipose TNF-alpha and MCP-1 mRNA and protein levels were elevated one-to twofold, in association with increased macrophage infiltration into the adipose tissue. When the rats were treated with a nonselective beta-adrenergic receptor blocker, propranolol, before induction of cerebral ischemic injury, the acute stroke-induced increase in TNF-alpha and MCP-1 was blocked, and fasting blood insulin concentration and homeostasis model assessment-insulin resistance were decreased. These results suggest a potential role of adipose proinflammatory cytokines induced by the sympathetic nervous system in the pathogenesis of glucose metabolic disorder in rats with acute ischemic stroke.
URI: http://hdl.handle.net/11455/67865
ISSN: 0193-1849
文章連結: http://dx.doi.org/10.1152/ajpendo.00301.2010
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