Suppr超能文献

一种用于在小鼠中进行美味饮食交替的行为和药理学特征描述。

A behavioral and pharmacological characterization of palatable diet alternation in mice.

机构信息

Laboratory of Addictive Disorders, Departments of Pharmacology and Experimental Therapeutics and Psychiatry, Boston University School of Medicine, Boston, MA, USA; Graduate Program for Neuroscience, Boston University School of Medicine, Boston, MA, USA.

Laboratory of Addictive Disorders, Departments of Pharmacology and Experimental Therapeutics and Psychiatry, Boston University School of Medicine, Boston, MA, USA.

出版信息

Pharmacol Biochem Behav. 2017 Dec;163:1-8. doi: 10.1016/j.pbb.2017.10.013. Epub 2017 Oct 31.

Abstract

Obesity and eating disorders are widespread in Western societies. Both the increased availability of highly palatable foods and dieting are major risk factors contributing to the epidemic of disorders of feeding. The purpose of this study was to characterize an animal model of maladaptive feeding induced by intermittent access to a palatable diet alternation in mice. In this study, mice were either continuously provided with standard chow food (Chow/Chow), or provided with standard chow for 2days and a high-sucrose, palatable food for 1day (Chow/Palatable). Following stability of intake within the cycling paradigm, we then investigated the effects of several pharmacological treatments on excessive eating of palatable food: naltrexone, an opioid receptor antagonist, SR141716A, a cannabinoid-1 receptor antagonist/inverse agonist, and BD-1063, a sigma-1 receptor antagonist. Over successive cycles, Chow/Palatable mice showed an escalation of palatable food intake within the first hour of renewed access to palatable diet and displayed hypophagia upon its removal. Naltrexone, SR141716A, and BD-1063 all reduced overconsumption of palatable food during this first hour. Here we provide evidence of strong face and convergent validity in a palatable diet alternation model in mice, confirming multiple shared underlying mechanisms of pathological eating across species, and thus making it a useful therapeutic development tool.

摘要

肥胖和饮食失调在西方社会普遍存在。高度美味的食物的可获得性增加和节食是导致进食障碍流行的主要危险因素。本研究的目的是描述一种通过间歇性接触美味饮食交替在小鼠中引起适应性进食障碍的动物模型。在这项研究中,小鼠要么连续提供标准的食物(Chow/Chow),要么提供标准食物 2 天,然后提供高蔗糖的美味食物 1 天(Chow/Palatable)。在循环范式内摄入量稳定后,我们研究了几种药物治疗对美味食物过度摄入的影响:纳曲酮,一种阿片受体拮抗剂;SR141716A,一种大麻素-1 受体拮抗剂/反向激动剂;BD-1063,一种 sigma-1 受体拮抗剂。在连续的循环中,Chow/Palatable 组小鼠在重新接触美味饮食的第一个小时内显示出美味食物摄入量的增加,并在其被移除时表现出摄食量减少。纳曲酮、SR141716A 和 BD-1063 都减少了在这第一个小时内对美味食物的过度摄入。在这里,我们在小鼠的美味饮食交替模型中提供了强烈的表面和收敛有效性的证据,证实了跨物种病理性进食的多个共同潜在机制,因此使其成为一种有用的治疗开发工具。

相似文献

引用本文的文献

1
Current perspectives on brain circuits involved in food addiction-like behaviors.当前对涉及食物成瘾样行为的大脑回路的观点。
J Neural Transm (Vienna). 2024 May;131(5):475-485. doi: 10.1007/s00702-023-02732-4. Epub 2024 Jan 12.
7
The histamine H receptor inverse agonist pitolisant reduces body weight in obese mice.组胺 H 受体反向激动剂匹哚尼沙明可降低肥胖小鼠的体重。
Naunyn Schmiedebergs Arch Pharmacol. 2018 Aug;391(8):875-881. doi: 10.1007/s00210-018-1516-2. Epub 2018 May 25.

本文引用的文献

1
Neuropharmacology of compulsive eating.强迫性进食的神经药理学。
Philos Trans R Soc Lond B Biol Sci. 2018 Mar 19;373(1742). doi: 10.1098/rstb.2017.0024.
2
Neuroscience of Compulsive Eating Behavior.强迫性进食行为的神经科学
Front Neurosci. 2017 Aug 24;11:469. doi: 10.3389/fnins.2017.00469. eCollection 2017.
3
Sigma Receptors and Substance Use Disorders.西格玛受体与物质使用障碍
Adv Exp Med Biol. 2017;964:177-199. doi: 10.1007/978-3-319-50174-1_13.
4
Sigma Receptors and Alcohol Use Disorders.西格玛受体与酒精使用障碍
Handb Exp Pharmacol. 2017;244:219-236. doi: 10.1007/164_2016_97.
5
Pathological Overeating: Emerging Evidence for a Compulsivity Construct.病理性暴饮暴食:强迫性结构的新证据
Neuropsychopharmacology. 2017 Jun;42(7):1375-1389. doi: 10.1038/npp.2016.269. Epub 2016 Dec 6.
6
Obesity: Current and potential pharmacotherapeutics and targets.肥胖症:当前及潜在的药物治疗方法与靶点
Pharmacol Ther. 2017 Feb;170:116-147. doi: 10.1016/j.pharmthera.2016.10.015. Epub 2016 Oct 20.
7
The role of the opioid system in binge eating disorder.阿片类系统在暴饮暴食症中的作用。
CNS Spectr. 2015 Dec;20(6):537-45. doi: 10.1017/S1092852915000668. Epub 2015 Oct 26.
8
Ethanol-related behaviors in mice lacking the sigma-1 receptor.缺乏σ-1受体的小鼠的乙醇相关行为
Behav Brain Res. 2016 Jan 15;297:196-203. doi: 10.1016/j.bbr.2015.10.013. Epub 2015 Oct 14.
10
Roles for the endocannabinoid system in ethanol-motivated behavior.内源性大麻素系统在乙醇诱导行为中的作用。
Prog Neuropsychopharmacol Biol Psychiatry. 2016 Feb 4;65:330-9. doi: 10.1016/j.pnpbp.2015.06.011. Epub 2015 Jun 26.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验