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5-羟色胺受体在皮质酮介导的食物摄取中的作用。

The role of 5-HT receptor on corticosterone-mediated food intake.

作者信息

Ge Tongtong, Zhang Zhuo, Lv Jiayin, Song Yunong, Fan Jie, Liu Wei, Wang Xuefeng, Hall F Scott, Li Bingjin, Cui Ranji

机构信息

Jilin Provincial Key Laboratory on Molecular and Chemical Genetics, The Second Hospital of Jilin University, Changchun, Jilin, 130041, People's Republic of China.

Department of Orthopedics, China-Japan Union Hospital of Jilin University 126 Xiantai Street, Nanguan District, Changchun, 13033, People's Republic of China.

出版信息

J Biochem Mol Toxicol. 2017 Jun;31(6). doi: 10.1002/jbt.21890. Epub 2017 Feb 10.

DOI:10.1002/jbt.21890
PMID:28186389
Abstract

Corticosterone plays an important role in feeding behavior. However, its mechanism remains unclear. Therefore, the present study aimed to investigate the effect of corticosterone on feeding behavior. In this study, cumulative food intake was increased by acute corticosterone administration in a dose-dependent manner. Administration of the 5-HT receptor agonist m-chlorophenylpiperazin (mCPP) reversed the effect of corticosterone on food intake. The anorectic effects of mCPP were also blocked by the 5-HT receptor antagonist RS102221 in corticosterone-treated mice. Both corticosterone and mCPP increased c-Fos expression in hypothalamic nuclei, but not the nucleus of the solitary tract. RS102221 inhibited c-Fos expression induced by mCPP, but not corticosterone. In addition, mCPP had little effect on TH and POMC levels in the hypothalamus. Furthermore, mCPP antagonized decreasing effect of the leptin produced by corticosterone. Taken together, our findings suggest that 5-HT receptors and leptin may be involved in the effects of corticosterone-induced hyperphagia.

摘要

皮质酮在摄食行为中起重要作用。然而,其机制仍不清楚。因此,本研究旨在探讨皮质酮对摄食行为的影响。在本研究中,急性给予皮质酮以剂量依赖性方式增加了累积食物摄入量。给予5-羟色胺(5-HT)受体激动剂间氯苯哌嗪(mCPP)可逆转皮质酮对食物摄入的影响。在接受皮质酮治疗的小鼠中,5-HT受体拮抗剂RS102221也阻断了mCPP的厌食作用。皮质酮和mCPP均增加了下丘脑核团中c-Fos的表达,但孤束核未增加。RS102221抑制了mCPP诱导的c-Fos表达,但未抑制皮质酮诱导的c-Fos表达。此外,mCPP对下丘脑酪氨酸羟化酶(TH)和促黑素细胞激素原(POMC)水平影响不大。此外,mCPP拮抗了皮质酮产生的瘦素的降低作用。综上所述,我们的研究结果表明,5-HT受体和瘦素可能参与了皮质酮诱导的摄食过多的作用。

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