Effect of Orexin-A on Post-ischemic Glucose Intolerance and Neuronal Damage

DOI Web Site PubMed 被引用文献20件 参考文献62件
  • Harada Shinichi
    Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Japan
  • Fujita-Hamabe Wakako
    Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Japan
  • Tokuyama Shogo
    Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Japan

この論文をさがす

抄録

Orexin-A is a newly identified neuropeptide expressed in the lateral areas of the hypothalamus that plays a role in various physiological functions, including regulation of glucose metabolism. We have previously reported that the development of post-ischemic glucose intolerance is one of the triggers of ischemic neuronal damage. Therefore, the aim of this study was to determine the effects of orexin-A 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. Neuronal damage was estimated by histological and behavioral analysis after MCAO. Intracerebroventricular administration of orexin-A (2.5, 25, or 250 pmol/mouse) significantly and dose-dependently suppressed the development of post-ischemic glucose intolerance on day 1 after MCAO and neuronal damage on day 3 after MCAO. In the liver and skeletal muscle, the expression levels of insulin receptor were decreased, whereas those of gluconeogenic enzymes were increased on day 1 after MCAO. Furthermore, these expressions were completely recovered to normal levels by orexin-A and were reversed by the administration of SB334867, a specific orexin-1 receptor antagonist. These results suggest that regulation of post-ischemic glucose intolerance by orexin-A suppressed cerebral ischemic neuronal damage.

収録刊行物

被引用文献 (20)*注記

もっと見る

参考文献 (62)*注記

もっと見る

関連プロジェクト

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ