PMID- 20978230
OWN - NLM
STAT- MEDLINE
DCOM- 20110131
LR  - 20220317
IS  - 1522-1555 (Electronic)
IS  - 0193-1849 (Linking)
VI  - 300
IP  - 1
DP  - 2011 Jan
TI  - Adipose proinflammatory cytokine expression through sympathetic system is 
      associated with hyperglycemia and insulin resistance in a rat ischemic stroke 
      model.
PG  - E155-63
LID - 10.1152/ajpendo.00301.2010 [doi]
AB  - 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.
FAU - Wang, Ya-Yu
AU  - Wang YY
AD  - Division of Family Medicine, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
FAU - Lin, Shih-Yi
AU  - Lin SY
FAU - Chuang, Yu-Han
AU  - Chuang YH
FAU - Chen, Chun-Jung
AU  - Chen CJ
FAU - Tung, Kwong-Chung
AU  - Tung KC
FAU - Sheu, Wayne Huey-Herng
AU  - Sheu WH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101026
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Adrenergic beta-Antagonists)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adipose Tissue, White/drug effects/*metabolism/pathology
MH  - Adrenergic beta-Antagonists/pharmacology
MH  - Animals
MH  - Brain Ischemia/blood/metabolism/*physiopathology
MH  - Chemokine CCL2/genetics/metabolism
MH  - Cytokines/blood/genetics/*metabolism
MH  - Gene Expression Regulation/drug effects
MH  - Glucose Intolerance/etiology
MH  - Hyperglycemia/blood/etiology/*metabolism
MH  - Inflammation Mediators/metabolism
MH  - *Insulin Resistance
MH  - Macrophages/metabolism
MH  - Male
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Stroke/blood/metabolism/*physiopathology
MH  - Sympathetic Nervous System/drug effects/*physiology
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
EDAT- 2010/10/28 06:00
MHDA- 2011/02/01 06:00
CRDT- 2010/10/28 06:00
PHST- 2010/10/28 06:00 [entrez]
PHST- 2010/10/28 06:00 [pubmed]
PHST- 2011/02/01 06:00 [medline]
AID - ajpendo.00301.2010 [pii]
AID - 10.1152/ajpendo.00301.2010 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2011 Jan;300(1):E155-63. doi: 
      10.1152/ajpendo.00301.2010. Epub 2010 Oct 26.