Involvement of hypothalamic PI3K-STAT3 signalling in regulating appetite suppression mediated by amphetamine.

doi:10.1111/bph.12667

中山醫學大學機構典藏 CSMUIR > 醫學院 > 生化微生物免疫研究所 > 期刊論文 > Item 310902500/11427

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题名:	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
贡献者:	中山醫學大學
关键词:	NPY;PI3K;POMC;STAT3;appetite;brain
日期:	2014
上传时间:	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.
显示于类别:	[生化微生物免疫研究所] 期刊論文

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