中山醫學大學機構典藏 CSMUIR:Item 310902500/11427
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    題名: Involvement of hypothalamic PI3K-STAT3 signalling in regulating appetite suppression mediated by amphetamine.
    作者: Chu, SC
    Chen, PN
    Hsieh, YS
    Yu, CH
    Lin, MH
    Lin, YH
    Kuo, DY
    貢獻者: 中山醫學大學
    關鍵詞: NPY;PI3K;POMC;STAT3;appetite;brain
    日期: 2014
    上傳時間: 2015-07-21T04:24:24Z (UTC)
    ISSN: 0007-1188
    摘要: BACKGROUND AND PURPOSE:
    Appetite suppression induced by amphetamine has been attributed to its inhibition of neuropeptide Y (NPY) neurons and activation of pro-opiomelanocortin (POMC) neurons in the hypothalamus. This study examined whether STAT3 was involved in these actions of amphetamine.
    EXPERIMENTAL APPROACH:
    Rats were given amphetamine daily for 4 days. Changes in the expression of NPY, POMC, melanocortin MC3 receptors, PI3K and STAT3 in the hypothalamus were assessed by RT-PCR and Western blotting. Antisense oligonucleotides to STAT3 were also used.
    KEY RESULTS:
    Expression of NPY decreased with a maximum effect day 2 of amphetamine treatment. Expression of POMC, MC3 receptors, PI3K and STAT3 increased with a maximum response on day 2. Moreover, phosphorylation of STAT3 and its DNA binding activity increased and was expressed in a similar pattern. Infusion (i.c.v.) of STAT3 antisense at 60 min before amphetamine treatment, partly blocked amphetamine-induced anorexia and modulated expression of NPY, POMC, MC3 receptors and PI3K, indicating the involvement of STAT3 in amphetamine-treated rats.
    CONCLUSIONS AND IMPLICATIONS:
    Hypothalamic PI3K-STAT3 signalling participated in the regulation of NPY- and POMC-mediated appetite suppression. These findings may contribute to a better understanding of anorectic drugs.
    © 2014 The British Pharmacological Society.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11427
    http://dx.doi.org/10.1111/bph.12667
    關聯: Br J Pharmacol. 2014 Jul;171(13):3223-33.
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