Ameliorating Effect of Hypothalamic Brain-Derived Neurotrophic Factor Against Impaired Glucose Metabolism After Cerebral Ischemic Stress in Mice

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Abstract

Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, has potent neuroprotective effects against brain injury. We recently reported that glucose intolerance/hyperglycemia could be induced by ischemic stress (i.e., post-ischemic glucose intolerance) following ischemic neuronal damage. Therefore, the aim of this study was to determine the effects of BDNF on the development of post-ischemic glucose intolerance and ischemic neuronal damage. Male ddY mice were subjected to middle cerebral artery occlusion (MCAO) for 2 h. On day 1, the expression levels of BDNF were significantly decreased in the cortex, hypothalamus, liver, skeletal muscle, and pancreas. The expression levels of tyrosine kinase B receptor, a BDNF receptor, decreased in the hypothalamus and liver and increased in the skeletal muscle and pancreas, but remained unchanged in the cortex. Intrahypothalamic administration of BDNF (50 ng/mouse) suppressed the development of post-ischemic glucose intolerance on day 1 and neuronal damage on day 3 after MCAO. In the liver and skeletal muscle, the expression levels of insulin receptors decreased, while gluconeogenic enzyme levels increased on day 1 after MCAO. These changes completely recovered to normal levels in the presence of BDNF. These results indicate that regulation of post-ischemic glucose intolerance by BDNF may suppress ischemic neuronal damage.

Journal

  • Journal of Pharmacological Sciences

    Journal of Pharmacological Sciences 118(1), 109-116, 2012-01-20

    The Japanese Pharmacological Society

References:  31

Cited by:  1

Codes

  • NII Article ID (NAID)
    10030454384
  • NII NACSIS-CAT ID (NCID)
    AA11806667
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    13478613
  • NDL Article ID
    023388062
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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