Alteration of Leptin-Induced STAT3 Activation in the Brain of Senescence-Accelerated Mouse (SAM) P8

  • Hosoi Toru
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University Department of Pharmacotherapy, Graduate School of Biomedical Sciences, Hiroshima University
  • Okuma Yasunobu
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University Department of Pharmacology, Faculty of Pharmaceutical Sciences, Chiba Institute of Science
  • Ono Atsushi
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University
  • Nomura Yasuyuki
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University Daiichi University, College of Pharmaceutical Sciences

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We used senescence-accelerated mouse prone 8 (SAMP8), a useful model of accelerated aging, to investigate the responsiveness to leptin with aging. The state of leptin-induced STAT3 phosphorylation in the hypothalamus was found to be higher in SAMP8 than in SAMR1, a control mouse showing normal aging, at 14—18 months of age but not at 2 months of age. Moreover, leptin receptor Ob-Rb expression in the hypothalamus was up-regulated in SAMP8. The results indicate that leptin sensitivity increases with aging in the SAM mouse brain.

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